Infectious cancer preserves dog genes for 11,000 years

Call it the Methuselah mutt. There are genes from a dog that lived 11,000 years ago in an infectious cancer that forms tumours on the genitals of dogs today. The cancer genes therefore preserve information about early domesticated dogs.

Canine transmissible venereal tumour (CTVT) is one of only two known mammalian cancers that can move from animal to animal through physical contact. The other is a cancer transmitted between Tasmanian devils when they bite each other. A genetic analysis suggests that CTVT originated about 11,000 years ago, surviving the millennia by moving from dog to dog during mating.

"These tumours are in dogs all around the world, yet they all originate from one single dog that lived all those years ago," says Elizabeth Murchison of the Wellcome Trust Sanger Institute in Hinxton, UK. Her team analysed DNA from two dogs with CTVT, one from Australia and one from Brazil.

"It's such a strange entity," says Murchison. "It's a cancer that's become a parasite, and yet it came from the same species that is now its host."

Cancer clones Modern CTVT cells are clones of the original cancer, but over the millennia they have accumulated almost 2 million unique mutations through mistakes in cell duplication. By contrast, human tumours typically have just 1000 to 5000, says Murchison, because they are not transmissible so only live a few decades at most.

These mutations revealed CTVT's age. By studying how many there were and working out the order and rate they appeared, the team calculated that the mother parasitic cell emerged 11,000 years ago. That is long after dogs first became domesticated, which may have happened as far back as 33,000 years ago.

"It's intriguing how a tumour has survived for more than 10,000 years travelling round and infecting a very large number of dogs," says Kerstin Lindblad-Toh of the Broad Institute in Cambridge, Massachusetts, head of the first team to sequence a dog's genome in 2005. "If more examples [of transmissible cancers] were found, it would be interesting to see what genetic changes characterise this type of long-lived tumour."

The samples taken from the Australian dog and the Brazilian dog seem to have diverged from one another about 500 years ago, at the height of European expansion. "It means that the cancer lived in just one small population of dogs for 10,500 years, but dogs carrying it were then picked up by explorers or seafarers who spread them, and the cancers they carried, all round the world," says Murchison.

Apart from the mutations, the DNA in CTVT is identical to that of the dog in which it originated. By comparing the DNA in CTVT cells with DNA from modern dogs and wolves, Murchison pieced together what the first infected canine probably looked like.

"We put together a genetic identikit of the dog," says Murchison. "It probably had a browny-grey agouti coat, a pointy snout, prickly ears, short hair, and was a dog, not a wolf," she says. It was most similar to modern huskies and Alaskan malamutes, but its closest relatives may now be extinct.

Origin of cancer

Murchison says the cancer probably evolved in a badly inbred population, in which the cancer cells passed between the animals during sex, but were overlooked by the immune system because the dogs were so closely related.

This lack of genetic diversity is the reason that the other known transmissible cancer spreads between Tasmanian devils. But the Tasmanian devil cancer is 30 years old at most.

CTVT is not an aggressive cancer and is easily curable in 90 per cent of cases, says Murchison. This may be because a mild form has evolved and adapted itself to life in its dog hosts. She adds that CTVT will probably go on for thousands more years, but may eventually go extinct if the cancer cells acquire too many mutations, which would cripple them.

No cancers of this kind have ever developed in people, but if they did, information from the Tasmanian devils and CTVT could help stop them, says Michael Stratton, also at the Wellcome Trust Sanger Institute.

Journal reference: Science, DOI: 10.1126/science.1247167

ORIGINAL: New Scientist

by Andy Coghlan 

23 January 2014

When a Disease is Genetic But Not Inherited: Bea Rienhoff’s Story

ORIGINAL: PLoS Blog
By Ricki Lewis, PhD
Posted: July 4, 2013

Hugh Rienhoff, dad and physician/geneticist, used exome sequencing to find his daughter Bea’s mutation. (Leah Fasten)

Genetics is the study of genes, DNA, and variation; heredity is the passing of inherited traits from parents to offspring. Families with one member, typically a child, who has a collection of unusual symptoms that don’t fit any clinical diagnosis may in fact have a genetic disease – but one that arose spontaneously in the child, rather than having been inherited from carrier parents.

Exome sequencing is helping to solve these genetics-but-not-heredity mysteries. The story of one little girl and her father’s efforts to find her mutant gene, and how the tale wove in and out and now back into my Human Genetics textbook, provides a beautiful illustration of the evolution of personalized genomic medicine.

THE BEA PROJECT
When Hugh Rienhoff first saw his daughter Bea, born in December 2003, he knew something was wrong. Her long feet, clenched fingers, poor muscle tone, widely-spaced hazel eyes, and a facial birthmark might have been just peculiarities to anyone who wasn’t also a physician and a geneticist.

As she grew into toddlerhood, Bea’s slow weight gain and bird-like legs reminded her father of Marfan syndrome. A little later, her divided uvula, the thing that hangs down in the throat, echoed the related Loeys-Dietz syndrome, both disorders of connective tissue.

(photo: Leah Fasten)

When Bea’s diagnosis remained elusive, Dr. Rienhoff bought secondhand DNA sequencing equipment, hired a lab to sample his daughter’s blood, and got to work in his home. “It was eerie examining her DNA, as though I were peering through a powerful microscope looking deep into my daughter while she patiently lay on the microscope stage, looking up, hoping for answers,” he said. But he isn’t the average citizen-scientist – he’s a researcher at Children’s Hospital Oakland Research Institute in San Francisco.

Bea’s journey to a diagnosis in what would be dubbed The Bea Project chronicles human genomics in the 21rst century. First Dr. Rienhoff probed variants of the genes behind the suspect Marfan and Loeys-Dietz syndromes, and a few others. When Bea didn’t have “atypical presentations” of those diseases, her father looked at genes that she expressed but that the other family members didn’t — the transcriptome of mRNAs. A few leads didn’t pan out.

 
REWRITING THE TEXTBOOKS
When I read Brendan Maher’s compelling article in Nature in fall 2007 about the Rienhoffs, while I was writing the 9th edition of my textbook, I thought their story would make a great intro for chapter 4, Mendelian Genetics. I too thought she had a genetic condition, likely inherited from carrier parents.

Chapter 4 opened with the story of the father seeking his daughter’s DNA. The book has lots of true tales of parents helping kids with genetic diseases, but the Rienhoffs were different, among the first, if not the first, to practice what’s now called do-it-yourself genetics.

(An aside here on textbooks. We authors actually do update new editions. I receive many reviews for each chapter, from instructors, and I rewrite extensively. Like evolution, the chapters go through many iterations, as I jettison what’s outdated or unclear, and keep what works, always updating, in a pedagogical survival of the fittest. Yes, the cost to the consumer is outrageous, but I have nothing to do with that, and rented and used books take my tiny royalty share. I wrote a short, cheap human genetics book as an alternative, but it was pirated and posted, by a company that does this routinely hoping authors won’t use Google Alerts. So it goes.)

Back to Bea. Some reviewers of the 9th edition of my textbook, as enchanted as they were by the story, requested I remove it. The reason: as the only one in her family with the strange symptoms, her condition might not have been inherited, and therefore wasn’t a good introduction to a chapter on single-gene (Mendelian) inheritance.

I reluctantly concurred. Out went the essay on Bea and her father’s quest to find a DNA sequence that could explain her odd collection of symptoms. Every few months I’d google them to see what progress they’d made. Misha Angrist, from whom I spontaneously inherited this blog, details Bea’s story in his 2011 book Here Is a Human-Being: At the Dawn of Personal Genomics/.

THE POWER OF EXOME SEQUENCING

(NHGRI)

After comparing transcriptomes (expressed genes) didn’t reveal Bea’s difference from her parents and brothers, Dr. Rienhoff turned to whole exome sequencing, with the help of Illumina. Beginning with the famous case of young Nicholas Volker in 2008 and his intestinal disease that turned out to be an immune system dysfunction, exome sequencing has provided diagnoses for a growing number of families in which a child’s symptoms don’t match a clinically recognized condition, nor are the parents carriers for a known inherited disease.

Exome studies compare the protein-encoding parts of the genome among all members of a family, seeking something that can explain the symptoms of the affected relative. Such mutations must be “non-synonymous,” which means that the protein’s amino acid sequence is altered, not just the DNA sequence. The genetic code (the correspondence between gene and protein, not to be confused with DNA or genome sequence, which it often is) includes redundant DNA triplets (codons) that encode the same amino acid, such as CTC, CTG, CTA and CTT all encoding leucine. These are “synonymous” codons because a mutation from one to another won’t change the protein, and therefore can’t affect the trait – it’s “silent.” A CTC mutated to a CTT still tells the cell to stick a leucine into the protein.

In the case of Nicholas Volker, the family’s exome sequencing found the causative mutation on his mother’s X chromosome — X-linked inheritance. The most common situation is to detect a mutation that both parents carry – autosomal recessive inheritance. The Rienhoff family had the third mode of inheritance – autosomal dominant. Textbookese. Can’t help it.

Bea is a yellow belt in kung fu (Leah Fasten)

BEA’S MUTATION
Exome sequencing revealed that Bea’s condition is indeed genetic, but she didn’t inherit it. She originated it. Bea Rienhoff, like all of us, harbors a handful of spontaneous “de novo” mutations that bloomed into existence, perhaps by slipping DNA replication enzymes, in her mother’s egg or her father’s sperm.

Brendan Maher follows up this chapter of Bea’s journey – finding her mutation — in a recent Nature article, and a technical account from Dr. Rienhoff and his colleagues will appear in the American Journal of Medical Genetics. 

The mutation lies in the transforming growth factor–B3 (TGF–B3) gene, which is indeed related to the pathways affected in Marfan and Loeys-Dietz syndromes, as Dr. Rienhoff suspected. A single-base change in Bea’s gene — a guanine replaced with adenine at position 1226 — replaces a cysteine with a tyrosine in the amino acid sequence.

Hugh Rienhoff and his wife Lisa Hane aren’t carriers, and their daughter’s mutation is dominant. Should she have children, each will face a 50:50 chance of inheriting what may become known as Rienhoff syndrome.

Bea’s condition – she’s still the only one known to have it, and I wouldn’t exactly call it a disease — has three defining characteristics: low muscle mass, growth retardation, and bent hands and feet. Her cells don’t make enough of the encoded growth factor, and the effects were set into motion when she was an embryo and her cells were sorting themselves into tissues and organs, particularly her muscles.

Dr. Rienhoff’s deepest concern, that his daughter’s condition would include the weakened cardiac blood vessels prone to balloon, and burst, as they do in Marfan syndrome, happily hasn’t happened and likely won’t. Bea is in many ways a normal and happy little girl, if small. And she’s a symbol of the new power of personalized genomic medicine.

Two Mutations Found to Have Triggered Evolutionary Leap 500 Million Years Ago In Humans

ORIGINAL: 33rdSquare
June 24, 2013

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A research team led by a University of Chicago scientist has discovered two key mutations that sparked a hormonal revolution 500 million years ago.

Evolution, it seems, sometimes jumps instead of crawls.

A research team led by a University of Chicago scientist has discovered two key mutations that sparked a hormonal revolution 500 million years ago.

In a feat of "molecular time travel," the researchers resurrected and analyzed the functions of the ancestors of genes that play key roles in modern human reproduction, development, immunity and cancer. By re-creating the same DNA changes that occurred during those genes' ancient history, the team showed that two mutations set the stage for hormones like estrogen, testosterone and cortisol to take on their crucial present-day roles.

"Changes in just two letters of the genetic code in our deep evolutionary past caused a massive shift in the function of one protein and set in motion the evolution of our present-day hormonal and reproductive systems," said Joe Thornton, PhD, professor of human genetics and ecology & evolution at the University of Chicago, who led the study.

"If those two mutations had not happened, our bodies today would have to use different mechanisms to regulate pregnancy, libido, the response to stress, kidney function, inflammation, and the development of male and female characteristics at puberty," Thornton said.

The findings were published online in the Proceedings of the National Academy of Sciences.

Tiny mutation may have shaped modern humans, scientists say

ORIGINAL: LATimes

By Eryn Brown, Los Angeles Times

February 14, 2013

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A genetic variant could have helped people survive crippling heat by giving them extra sweat glands, says a report from a team that sought to replicate the effect in mice.

About 30,000 years ago, a tiny mutation arose in a gene known as EDAR and began to spread rapidly in central China, eventually becoming common in the region.

This week, scientists at Harvard University offered some explanations for why the EDAR mutation may have been so successful — by observing how it affects mice, animals long used in disease research but never before pressed into service for the study of human evolution.

The small change, substituting one chemical letter of DNA for another, may have helped humans in Asia survive crippling heat and humidity by endowing them with extra sweat glands, the scientists reported Thursday in the journal Cell. It may also have made people with the mutation more attractive to the opposite sex by allowing them to grow thicker hair or fuller breasts.

The research showed how scientists are getting better at zeroing in on the key DNA changes that shaped who we are today. The analysis also revealed that mutations in genes involved in bone density, skin color and immune system function were likely pivotal in helping humans adapt to new environments as they spread throughout the world.

"You can let the genome tell you what's been important in human evolution," said Harvard computational geneticist Pardis Sabeti, senior author of the two studies published in Cell.

Living beings evolve through a process known as selection. Organisms with advantageous traits thrive, passing their DNA to another generation. Harmful traits die off when their hosts can't live long enough to reproduce.

Scientists can recognize patterns in DNA that indicate a particular version of a gene has spread through a population because it boosts survival. But those beneficial mutations are usually passed down along with thousands of other variants that happen to live in their chromosomal neighborhood.

That has made it hard for researchers to determine exactly which genetic tweaks conferred the competitive advantage.

"It's like you walk around a ghost town and you see the clues that something happened, but you don't know exactly what or how," said UC Santa Cruz biomolecular engineer Ed Green, who was not involved in the new studies.

Sabeti and an international group of colleagues are using multiple techniques to dig out the key drivers of human evolution in the avalanche of genetic data made possible by faster, cheaper sequencing technology. A single human genome contains 3 billion pairs of the chemical letters A, C, G and T.

To sort through all that, the researchers used powerful computers to identify genetic changes that seemed to be linked to evolutionary change. They examined the DNA of 179 people from Utah, East Asia and West Africa and revealed hundreds of potentially key variants, including mutations that made bones stronger and helped people absorb more vitamin D from the sun as they moved to northern latitudes.

Sabeti wanted to understand more about how these mutations influenced human traits. Such work requires experimentation — and that is where the mice entered the picture.

The EDAR gene was already known to influence hair thickness and to alter tooth shape in humans. But Sabeti wasn't sure whether the mutation her team turned up was a key change that drove human evolution.

To arrive at an answer, she and her collaborators genetically engineered mice that had the Asian version of EDAR.

They found that, as with humans, the mice had thicker hair than their counterparts without the variant. They also displayed traits the researchers hadn't expected to see, including more sweat glands and changes in their mammary glands. (The variant had no discernible effect on the animals' teeth.)

Next, the team examined the fingertips and EDAR genes of 623 people in Taizhou, China, to see if those who had the mutation also had a larger number of active sweat glands. They did.

The results present a fuller picture of how the EDAR mutation may have helped drive evolution.

People who inherited the variant may have reproduced more successfully because having more sweat glands helped their bodies cool off in hot, humid weather.

Or it might have spread through sexual selection. Thicker hair may have been more appealing in a mate. In addition, the mutation could have changed breast size or shape, making people who had it more attractive to the opposite sex.

That scientists could study a mouse and reveal such insights into human evolution was "amazing," said Green, who co-wrote an essay about the work that was also published in Cell on Thursday.

The story was similar for the TLR-5 gene, which is involved in protecting the body from certain bacteria. Instead of testing in mice, the scientists used cell cultures in lab dishes to demonstrate that the mutation reduced the immune system's inflammatory response to a key protein in the bacterial pathogens.

The team's analysis suggested that many of the key genetic changes weren't in genes themselves, but in regions of the chromosome that scientists think contain instructions for how those genes should be turned on and off, or tuned up or down, Sabeti said.

The work offers a long-awaited view into the key mutations that billions of us share and that made us who we are, said David Kingsley, an evolutionary geneticist at Stanford University who was not involved in the new studies.

"We're reading a book of information about our past that has never been available before," he said.

eryn.brown@latimes.com

Berkeley researchers find evidence for a "molecular fountain of youth"

ORIGINAL: GizMag

By Brian Dodson

February 5, 2013

The SIRT3 protein molecule that appears to play a central role in regulating aging and longevity

The quest for longer and healthier life, if not immortality, has been part of the human experience since we evolved the ability to recognize the total annihilation of individual death. Our understanding of the biology of aging at the molecular level is advancing so rapidly that it appears inevitable that another decade or two of life will be enabled before long. A new step in what may be the right direction has just been published by researchers at the University of California, Berkeley.

The ravages of aging appear to be related to oxidative stress combined with telomere exhaustion, along with many other known and unknown factors. The subject of the new Berkeley study is a class of proteins called sirtuins that are known to play a central role in regulating aging and longevity in many non-human models (such as mice).

There is good evidence that these proteins also play a similar role in humans. For example, research has shown that, of two variants of the SIRT3 sirtuin protein (known to have strong anti-oxidant properties), humans who live past 90 years of age only have one of the variants in their bodies, the variant that enhances production of SIRT3. The difference between the two variants results from a change of one gene by one mutation, and appears to be sufficient to significantly affect an organism's longevity. This suggests a strong link between SIRT3 and longevity.

The genetics of longevity are quite interesting, but still more interesting would be finding an approach to offset the hand you were dealt at birth, or better yet, to stack the deck. The authors of the Berkeley study decided to see if SIRT3 could rejuvenate blood stem cells extracted from old mice.

Their first step was to see what happened as mice, which did not possess the SIRT3 gene, aged. When young, these "knockout" mice followed the same course of aging as did a set of normal control mice. However, when the mice were two years old (about an average lifespan for a lab mouse), the knockout mice had far fewer blood stem cells than did the control group.

What causes the difference in the course of aging? Young cells have low levels of oxidative stress (the generation of reactive oxygen species during metabolism), low enough that the body's normal anti-oxidants can keep up with the resulting damage. When they get older, they can't keep up, and need a boost of SIRT3 to help them. When there is no SIRT3, the progress of old age occurs sooner and more rapidly.

“When we get older, our system doesn’t work as well, and we either generate more oxidative stress or we can’t remove it as well, so levels build up,” said Chen. “Under this condition, our normal anti-oxidative system can’t take care of us, so that’s when we need SIRT3 to kick in to boost the anti-oxidant system. However, SIRT3 levels also drop with age, so over time, the system is overwhelmed.”

So it appears that age-related degeneration speeds up in the absence of SIRT3 in the system – at least among mice. The Berkeley team decided to see if increasing SIRT3 levels could rehabilitate the blood stem cells. This was done by infusing the blood stem cells with the SIRT3 protein, following which their ability to make new blood cells did indeed return.

Further studies will address if SIRT3-induced rejuvenation will apply to whole organisms, so that they might live longer when so treated, even after experiencing normal aging events.

Source: University of California at Berkeley

About the Author

From an early age Brian wanted to become a scientist. He did, earning a Ph.D. in physics and embarking on an R&D career which has recently broken the 40th anniversary. What he didn't expect was that along the way he would become a patent agent, a rocket scientist, a gourmet cook, a biotech entrepreneur, an opera tenor and a science writer. All articles by Brian Dodson

Genetic Mutation May Have Allowed Early Humans to Migrate Throughout Africa

ORIGINAL: ScienceDaily

ScienceDaily (Sep. 19, 2012) — A genetic mutation that occurred thousands of years ago might be the answer to how early humans were able to move from central Africa and across the continent in what has been called "the great expansion," according to new research from Wake Forest Baptist Medical Center.

A genetic mutation that occurred thousands of years ago might be the answer to how early humans were able to move from central Africa and across the continent in what has been called "the great expansion," according to new research. (Credit: © Sailorr / Fotolia)

By analyzing genetic sequence variation patterns in different populations around the world, three teams of scientists from Wake Forest Baptist, Johns Hopkins University School of Medicine and the University of Washington School of Medicine, Seattle, demonstrated that a critical genetic variant arose in a key gene cluster on chromosome 11, known as the fatty acid desaturase cluster or FADS, more than 85,000 years ago. This variation would have allowed early humans to convert plant-based polyunsaturated fatty acids (PUFAs) to brain PUFAs necessary for increased brain size, complexity and function. The FADS cluster plays a critical role in determining how effectively medium-chain PUFAs found in plants are converted to the long-chain PUFAs found in the brain.

This research is published online today in PLOS ONE.

Image: EVOLUTION

Archeological and genetic studies suggest that homo sapiens appeared approximately 180,000 years ago, but stayed in one location around bodies of water in central Africa for almost 100,000 years. Senior author Floyd H. "Ski" Chilton, Ph.D., professor of physiology and pharmacology and director of the Center for Botanical Lipids and Inflammatory Disease Prevention at Wake Forest Baptist, and others have hypothesized that this location was critical, in part, because early humans needed large amounts of the long-chain PUFA docosahexaenoic acid (DHA), which is found in shellfish and fish, to support complex brain function.

"This may have kept early humans tethered to the water in central Africa where there was a constant food source of DHA," Chilton said. "There has been considerable debate on how early humans were able to obtain sufficient DHA necessary to maintain brain size and complexity. It's amazing to think we may have uncovered the region of genetic variation that arose about the time that early humans moved out of this central region in what has been called the 'great expansion.'"

Once this trait arose, the study shows that it was under intense selective pressure and thus rapidly spread throughout the population of the entire African continent. "The power of genetics continually impresses me, and I find it remarkable that we can make inferences about things that happened tens of thousands of years ago by studying patterns of genetic variation that exist in contemporary populations," said Joshua M. Akey, Ph.D., lead scientist at the University of Washington.

This conversion meant that early humans didn't have to rely on just one food source, fish, for brain growth and development. This may have been particularly important because the genetic variant arose before organized hunting and fishing could have provided more reliable sources of long-chain PUFAs, Akey said.

To investigate the evolutionary forces shaping patterns of variation in the FADS gene cluster in geographically diverse populations, the researchers analyzed 1,092 individuals representing 15 different human populations that were sequenced as part of the 1000 Genome Project and 1,043 individuals from 52 populations from the Human Genome Diversity Panel database. They focused on the FADS cluster because they knew those genes code for the enzymatic steps in long-chain PUFA synthesis that are the least efficient.

Chilton said the findings were possible because of the collaboration of internationally recognized scientists from three distinct and diverse disciplines -- fatty acid biochemistry (Wake Forest Baptist), statistical genetics (Johns Hopkins) and population genetics (University of Washington). This new information builds on Chilton's 2011 research findings published in BMC Genetics that showed how people of African descent have a much higher frequency of the gene variants that convert plant-based medium-chain omega-6 PUFAs found in cooking oils and processed foods to long-chain PUFAs that cause inflammation. Compared to Caucasians, African Americans in the United States have much higher rates of hypertension, type 2 diabetes, stroke, coronary heart disease and certain types of cancer. "The current observation provides another important clue as to why diverse racial and ethnic populations likely respond differently to the modern western diet," Chilton said.

This research was supported by National Institutes of Health grants, P50 AT002782 and a Clinical and Translational Science Award grant to The Johns Hopkins Medical Institutions. Additional support was received from the Wake Forest Health Sciences Center for Public Health Genomics. Additional support came from the Mary Beryl Patch Turnbull Scholar Program and the MOSAIC initiative of Johns Hopkins University.

Chilton has a financial interest in and is a consultant for Gene Smart Health. His potential conflict of interest is being institutionally managed by Wake Forest Baptist and outside sponsors, as appropriate. No other authors have a conflict of interest.

First author is Rasika Mathias, Sc.D, assistant professor of medicine and epidemiology, Johns Hopkins; contributing authors include Hannah C. Ainsworth and Susan Sergeant, both of Wake Forest Baptist; Wenqing Fu, U of W; Dara G. Torgerson, University of California San Francisco; and Ingo Ruczinski and Kathleen C. Barnes of Johns Hopkins.

Biologists Reveal Potential 'Fatal Flaw' in Iconic Sexual Selection Study

ORIGINAL: Science Daily

A new sexual selection study replicates an iconic 1948 study and finds it flawed. The graphic shows that children of fruit fly parents with different mutations have an equal chance of inheriting just the mother's mutation, just the father's mutation, both mutations or neither mutation. (Credit: Kim DeRose)

ScienceDaily (June 26, 2012) — A classic study from more than 60 years ago suggesting that males are more promiscuous and females more choosy in selecting mates may, in fact, be wrong, say life scientists who are the first to repeat the historic experiment using the same methods as the original.

In 1948, English geneticist Angus John Bateman published a study showing that male fruit flies gain an evolutionary advantage from having multiple mates, while their female counterparts do not. Bateman's conclusions have informed and influenced an entire sub-field of evolutionary biology for decades.

"Bateman's 1948 study is the most-cited experimental paper in sexual selection today because of its conclusions about how the number of mates influences fitness in males and females," said Patricia Adair Gowaty, a distinguished professor of ecology and evolutionary biology at UCLA. "Yet despite its important status, the experiment has never been repeated with the methods that Bateman himself originally used, until now.

"Our team repeated Bateman's experiment and found that what some accepted as bedrock may actually be quicksand. It is possible that Bateman's paper should never have been published."

Gowaty's study was published June 11 in the online edition of Proceedings of the National Academy of Sciences and is scheduled for publication in an upcoming print edition.

The original experiment on Drosophila melanogaster, also known as the common fruit fly, was performed by creating multiple, isolated populations with either five males and five females or three of each gender in a jar. The insects mated freely in the experimental populations, and Bateman examined the children that made it to adulthood. To count the number of adult offspring engendered by each of his original insect subjects, Bateman needed a reliable way to match parents with children.

Nowadays, modern geneticists would use molecular evidence to determine the genetic parentage of each child, but DNA analysis was not available in the 1940s. Instead, Bateman chose his initial specimens carefully, selecting D. melanogaster flies that each had a unique, visible mutation that could be transferred from parent to child, Gowaty said.

The mutations were extreme. Some of the flies had curly wings, others thick bristles, and still others had eyes reduced in size to narrow slits. The outward differences in each breeding subject allowed Bateman to work backward to determine the parentage of some of the fly progeny and to document each mating pair among the original insects. A child with curly wings and thick bristles, for example, could only have come from one possible pairing.

Yet Bateman's method, which was cutting-edge for its time, had a "fatal flaw," according to Gowaty.

Imagine the child of a curly-winged mother and an eyeless father. The child has an equal chance of having both mutations, only the father's mutation, only the mother's mutation or no mutation at all. In order to know who mated with whom, Bateman used only the children with two mutations, because these were the only ones for which he could specifically identify both the mother and father. But by counting only the children with two mutations, Bateman probably got a skewed sample, Gowaty said. In repeating Bateman's experiment, she and her colleagues found that the flies with two severe mutations are less likely to survive into adulthood.

Flies use their wings not only to hover but also to sing during courtship, which is why curly wings present a huge disadvantage. Specimens with deformed eyes might have an even tougher time surviving. The 25 percent of children born with both mutations were even more likely to die before being counted by Bateman or Gowaty.

"It's not surprising that the kids died like flies when they got one dramatic mutation from mom and another dramatic mutation from dad," she said.

Gowaty found that the fraction of double-mutant offspring was significantly below the expected 25 percent, which means Bateman would have been unable to accurately quantify the number of mates for each adult subject. Further, his methodology resulted in more offspring being assigned to fathers than mothers, something that is impossible when each child must have both a father and a mother, Gowaty said.

Bateman concluded that male fruit flies produce many more viable offspring when they have multiple mates but that females produce the same number of adult children whether they have one mate or many. But Gowaty and her colleagues, by performing the same experiment, found that the data were decidedly inconclusive.

In their repetition -- and possibly in Bateman's original study -- the data failed to match a fundamental assumption of genetic parentage assignments. Specifically, the markers used to identify individual subjects were influencing the parameters being measured (the number of mates and the number of offspring). When offspring die from inherited marker mutations, the results become biased, indicating that the method is unable to reliably address the relationship between the number of mates and the number of offspring, said Gowaty. Nonetheless, Bateman's figures are featured in numerous biology textbooks, and the paper has been cited in nearly 2,000 other scientific studies.

"Here was a classic paper that has been read by legions of graduate students, any one of whom is competent enough to see this error," Gowaty said. "Bateman's results were believed so wholeheartedly that the paper characterized what is and isn't worth investigating in the biology of female behavior."

Repeating key studies is a tenet of science, which is why Bateman's methodology should have been retried as soon as it became important in the 1970s, she said. Those who blindly accept that females are choosy while males are promiscuous might be missing a big piece of the puzzle.

"Our worldviews constrain our imaginations," Gowaty said. "For some people, Bateman's result was so comforting that it wasn't worth challenging. I think people just accepted it."

Shaking the foundation

Biologists studying sexual selection examine mating habits of organisms ranging from fruit flies to gorillas, both in the lab and in the wild, in order to better understand how certain traits or behaviors confer evolutionary advantages.

Sexual selection began as a discipline following Charles Darwin's publication of "The Descent of Man, and Selection in Relation to Sex," considered Darwin's defense against critics of his theory of evolution through natural selection. He argued that while the unwieldy, colorful tails of peacocks hindered flight and made males easy targets for hungry tigers, the flamboyant plumage served a vital role in attracting potential mates. The overdressed birds had an unexpected evolutionary advantage that did not help when it came to escaping predators but did help when it came to producing offspring through sexual selection, said Gowaty.

Darwin, and later Bateman, cleaved to the notion that females of a species tended to be discriminating and passive, while the far more promiscuous males competed for their attentions. In the last few decades, however, evolutionary biologists have shown that the story is far more complicated. Gowaty, who has been interested in female mating habits in insects and birds since the beginning of her career, spent 30 years in the field studying Eastern bluebirds. She published the first molecular genetics study showing that females in a socially monogamous species mated outside their traditional pairs regularly.

Gowaty describes the benefits of multiple mates as an answer to the never-ending evolutionary struggle against what may be the world's greatest predator: disease.

"Our pathogens have much shorter generation times than we do as the hosts, and they evolve offenses much more rapidly than we can evolve defenses," she said. "One of the rules of nature is that our pathogens are going to get us."

In this illness-driven arms race, organisms that produce offspring from multiple mates are more likely to produce some children with the right antibodies to survive the next generation of viruses, bacteria and parasites. Fruit fly males are likely to give females the additional variation in the genome that they need to build strong immune systems in their kids, Gowaty said.

For Gowaty, there are many open questions remaining when it comes to female mating habits, whether in fruit flies or other organisms. Yet shaking the bedrock of the Bateman paradigm may help the field examine new perspectives.

"Paradigms are like glue, they constrain what you can see," she said. "It's like being stuck in sludge -- it's hard to lift your foot out and take a step in a new direction."

This study was federally funded by the National Science Foundation. Other co-authors included Wyatt Anderson, a professor of genetics at the University of Georgia and a member of the National Academy of Sciences, and Yong-Kyu Kim, a research scientist at Emory University.

Genetically Modified Grass Kills Cattle By Producing Warfare Chemical Cyanide

ORIGINAL: Natural Society

Anthony Gucciardi

June 24, 2012 

Another report of genetically modified creations taking the lives of livestock has hit the media, and this time genetically modified grass has been identified as the culprit according to CBS News. Shockingly (and quite disturbingly), the GM grass actually produced toxic cyanide and sent the cattle into a life-ending fit that included painful bellowing and convulsions. The deaths have led to a federal investigation centered in Central Texas, where the cattle had resided.

Just east of Austin, the cows lived on an 80-acre ranch owned by Jerry Abel. Abel says that the fields were used for over 15 years for cattle grazing and hay, and that the genetically modified grass was ‘tested’ previously and should have been ‘perfect’. The GM grass however, known as Tifton 85, appears have been producing toxic cyanide. Used as a genocidal agent in World War 2 by the Germans and considered to be an extremely dangerous substance internationally, it is extremely concerning that cyanide is now being produced by once harmless grass thanks to the modification process.

The 18 cattle went off to enjoy some ‘fresh’ new genetically modified grass, when Abel says they went into a fit of convulsions and shrieks. He explains:

“When our trainer first heard the bellowing, he thought our pregnant heifer may be having a calf or something,” said Abel. “But when he got down here, virtually all of the steers and heifers were on the ground. Some were already dead, and the others were already in convulsions.”

Within 15 hours of this incident, all of the cattle had died as a result of the grass ‘suddenly’ producing cyanide and therefore throwing them into a lethal fit. According to USDA scientists, it may be the result of a mutation — the same kind of mutation that has been seen in many of Monsanto’s Roundup-Ready crops.

What’s more is the fact that many other farmers are now testing their grounds and also finding the presence of cyanide. While there is not yet a large number of reports concerning cattle deaths from cyanide, it was recently revealed that one large biotech company Syngenta had been covering up further animal deaths from genetically modified corn.

Additional sources:

CDC Facts on Cyanide

Invertebrados que sobreviven a 2,000 metros de profundidad desafían la ciencia

ORIGINAL: Más Verde Digital

by masverde

Un equipo de investigadores españoles y rusos, organizado por el grupo Cavex de la Universidad de Moscú, ha encontrado en la cueva Krubera-Voronja, en la República de Abjasia (en el Cáucaso Oriental) unas criaturas que logran sobrevivir a más de 2.000 metros de profundidad.

Los científicos y espeleólogos descendieron a esta cueva con el objetivo de explorar sus formas de vida e hicieron un descubrimiento excepcional. Han encontrado a más de 12 especies de pequeños invertebrados, entre las cuales por lo menos cinco son nuevas para la ciencia, mientras que otras aún esperan por ser identificadas. Los primeros resultados del estudio fueron publicados en la revista ‘International Journal of Speleology’.

El hallazgo cuenta con pequeños escarabajos, pseudoescorpiones y colémbolos, milpiés y diferentes tipos de crustáceos y anfípodos. Según el biólogo Alberto Sendra, son muy parecidos a los que vivirían en cualquier jardín pero mutados para adaptarse a estas condiciones de profundidad.

“Ellos tienen una pobre alimentación, viven en una temperatura constante y una humedad relativa del 100%, algo que no resisten la mayoría de los artrópodos”.

“Este trabajo es importante porque presenta por primera vez la descripción de la comunidad de vida animal más profunda del mundo, un ecosistema único de los animales terrestres así como de los acuáticos”, indica Sendra.

Ya era conocida la existencia de bacterias a más de tres kilómetros bajo tierra, pero hasta ahora no había ninguna evidencia de la existencia de fauna a partir de 920 metros. Los investigadores planean volver a la cueva en 2013 para estudiar el nuevo ecosistema. “Estamos convencidos de que allí hay más sorpresas y ardemos en deseos de investigar más”, destaca Alberto Sendra

La cueva de Krubera-Voronja es la más profunda de la Tierra, que desciende verticalmente hasta los 2.191 metros de profundidad. Se encuentra en el valle glacial de Ortobalagan, en el macizo de Arabika, en Abjasia.

Fuente: RT, Agencias

Powerful new approach to attack flu virus

ORIGINAL: eScienceNews

An international research team has manufactured a new protein that can combat deadly flu epidemics. MSU photographer, Kurt Stepnitz

An international research team has manufactured a new protein that can combat deadly flu epidemics. The paper, featured on the cover of the current issue of Nature Biotechnology, demonstrates ways to use manufactured genes as antivirals, which disable key functions of the flu virus, said Tim Whitehead, assistant professor of chemical engineering and materials science at Michigan State University.

"Our most potent design has proven effective on the vulnerable sites on many pandemic influenza viruses, including several H1N1 (Spanish flu, Swine flu) and H5N1 (Avian flu) subtypes," said Whitehead, the paper's co-lead author. "These new therapeutics are urgently needed, so we were especially pleased to see that it neutralizes H1N1 viruses with potency."

From its earlier research, the team used computer-aided design to engineer proteins that targeted vulnerable sites on the highly adaptable virus. From there, researchers optimized their designer proteins by comprehensively mapping the mutations that gave the proteins a strong advantage when attacking the viruses' targeted areas.

The team improved its proteins through a process called "DNA deep sequencing." This allowed Whitehead and his colleagues to simultaneously sequence millions of variants of their manufactured proteins, identify and keep the beneficial mutations and optimize the proteins' performance.

"By taking only the best mutations, we can reprogram our proteins to burrow into viruses at key locations and render them harmless," he said. "Our work demonstrates a new approach to construct therapeutic proteins, which we hope will spur development of new protein drugs by the biopharmaceutical industry."

This research also laid the groundwork for future treatments of all flu viruses as well as other diseases such as smallpox, Whitehead added.

Whitehead's co-authors included researchers from the University of Washington, the Scripps Research Institute (La Jolla, Calif.), Naval Health Research Center (San Diego) and the Weizmann Institute of Science (Rehovot, Israel).

The research was funded by Defense Research Projects Agency, the Defense Threat Reduction Agency, the National Institutes of Health, the National Institute of Allergy and Infectious Diseases and the National Institute of General Medical Sciences.

Source: Michigan State University

Gulf of Mexico seafood deformities alarm scientists

ORIGINAL: AlJazzera

Dahr Jamail Last Modified: 18 Apr 2012 03:16

Eyeless shrimp and fish with lesions are becoming common, with BP oil pollution believed to be the likely cause.

New Orleans, LA - "The fishermen have never seen anything like this," Dr Jim Cowan told Al Jazeera. "And in my 20 years working on red snapper, looking at somewhere between 20 and 30,000 fish, I've never seen anything like this either."

Dr Cowan, with Louisiana State University's Department of Oceanography and Coastal Sciences started hearing about fish with sores and lesions from fishermen in November 2010.

Cowan's findings replicate those of others living along vast areas of the Gulf Coast that have been impacted by BP's oil and dispersants.

Gulf of Mexico fishermen, scientists and seafood processors have told Al Jazeera they are finding disturbing numbers of mutated shrimp, crab and fish that they believe are deformed by chemicals released during BP's 2010 oil disaster.

Along with collapsing fisheries, signs of malignant impact on the regional ecosystem are ominous: horribly mutated shrimp, fish with oozing sores, underdeveloped blue crabs lacking claws, eyeless crabs and shrimp - and interviewees' fingers point towards BP's oil pollution disaster as being the cause.

Eyeless shrimp

Tracy Kuhns and her husband Mike Roberts, commercial fishers from Barataria, Louisiana, are finding eyeless shrimp.

"At the height of the last white shrimp season, in September, one of our friends caught 400 pounds of these," Kuhns told Al Jazeera while showing a sample of the eyeless shrimp.

According to Kuhns, at least 50 per cent of the shrimp caught in that period in Barataria Bay, a popular shrimping area that was heavily impacted by BP's oil and dispersants, were eyeless. Kuhns added: "Disturbingly, not only do the shrimp lack eyes, they even lack eye sockets."

Eyeless shrimp, from a catch of 400 pounds of eyeless shrimp, said to be caught September 22, 2011, in Barataria Bay, Louisiana [Erika Blumenfeld/Al Jazeera]

"Some shrimpers are catching these out in the open Gulf [of Mexico]," she added, "They are also catching them in Alabama and Mississippi. We are also finding eyeless crabs, crabs with their shells soft instead of hard, full grown crabs that are one-fifth their normal size, clawless crabs, and crabs with shells that don't have their usual spikes … they look like they've been burned off by chemicals."

On April 20, 2010, BP's Deepwater Horizon oilrig exploded, and began the release of at least 4.9 million barrels of oil. BP then used at least 1.9 million gallons of toxic Corexit dispersants to sink the oil.

Keath Ladner, a third generation seafood processor in Hancock County, Mississippi, is also disturbed by what he is seeing.

"I've seen the brown shrimp catch drop by two-thirds, and so far the white shrimp have been wiped out," Ladner told Al Jazeera. "The shrimp are immune compromised. We are finding shrimp with tumors on their heads, and are seeing this everyday."

While on a shrimp boat in Mobile Bay with Sidney Schwartz, the fourth-generation fisherman said that he had seen shrimp with defects on their gills, and "their shells missing around their gills and head".

"We've fished here all our lives and have never seen anything like this," he added.

Ladner has also seen crates of blue crabs, all of which were lacking at least one of their claws.

Darla Rooks, a lifelong fisherperson from Port Sulfur, Louisiana, told Al Jazeera she is finding crabs "with holes in their shells, shells with all the points burned off so all the spikes on their shells and claws are gone, misshapen shells, and crabs that are dying from within … they are still alive, but you open them up and they smell like they've been dead for a week".

Rooks is also finding eyeless shrimp, shrimp with abnormal growths, female shrimp with their babies still attached to them, and shrimp with oiled gills.

"We also seeing eyeless fish, and fish lacking even eye-sockets, and fish with lesions, fish without covers over their gills, and others with large pink masses hanging off their eyes and gills."

Rooks, who grew up fishing with her parents, said she had never seen such things in these waters, and her seafood catch last year was "ten per cent what it normally is".

"I've never seen this," he said, a statement Al Jazeera heard from every scientist, fisherman, and seafood processor we spoke with about the seafood deformities.

Given that the Gulf of Mexico provides more than 40 per cent of all the seafood caught in the continental US, this phenomenon does not bode well for the region, or the country.

BP's chemicals?

"The dispersants used in BP's draconian experiment contain solvents, such as petroleum distillates and 2-butoxyethanol. Solvents dissolve oil, grease, and rubber," Dr Riki Ott, a toxicologist, marine biologist and Exxon Valdez survivor told Al Jazeera. "It should be no surprise that solvents are also notoriously toxic to people, something the medical community has long known".

The dispersants are known to be mutagenic, a disturbing fact that could be evidenced in the seafood deformities. Shrimp, for example, have a life-cycle short enough that two to three generations have existed since BP's disaster began, giving the chemicals time to enter the genome.

Pathways of exposure to the dispersants are inhalation, ingestion, skin, and eye contact. Health impacts can include headaches, vomiting, diarrhea, abdominal pains, chest pains, respiratory system damage, skin sensitisation, hypertension, central nervous system depression, neurotoxic effects, cardiac arrhythmia and cardiovascular damage. They are also teratogenic - able to disturb the growth and development of an embryo or fetus - and carcinogenic.

Cowan believes chemicals named polycyclic aromatic hydrocarbons (PAHs), released from BP's submerged oil, are likely to blame for what he is finding, due to the fact that the fish with lesions he is finding are from "a wide spatial distribution that is spatially coordinated with oil from the Deepwater Horizon, both surface oil and subsurface oil. A lot of the oil that impacted Louisiana was also in subsurface plumes, and we think there is a lot of it remaining on the seafloor".

Marine scientist Samantha Joye of the University of Georgia published results of her submarine dives around the source area of BP's oil disaster in the Nature Geoscience journal.

Her evidence showed massive swathes of oil covering the seafloor, including photos of oil-covered bottom dwelling sea creatures.

While showing slides at an American Association for the Advancement of Science annual conference in Washington, Joye said: "This is Macondo oil on the bottom. These are dead organisms because of oil being deposited on their heads."

Dr Wilma Subra, a chemist and Macarthur Fellow, has conducted tests on seafood and sediment samples along the Gulf for chemicals present in BP's crude oil and toxic dispersants.

"Tests have shown significant levels of oil pollution in oysters and crabs along the Louisiana coastline," Subra told Al Jazeera. "We have also found high levels of hydrocarbons in the soil and vegetation."

According to the US Environmental Protection Agency, PAHs "are a group of semi-volatile organic compounds that are present in crude oil that has spent time in the ocean and eventually reaches shore, and can be formed when oil is burned".

"The fish are being exposed to PAHs, and I was able to find several references that list the same symptoms in fish after the Exxon Valdez spill, as well as other lab experiments," explained Cowan. "There was also a paper published by some LSU scientists that PAH exposure has effects on the genome."

The University of South Florida released the results of a survey whose findings corresponded with Cowan's: a two to five per cent infection rate in the same oil impact areas, and not just with red snapper, but with more than 20 species of fish with lesions. In many locations, 20 per cent of the fish had lesions, and later sampling expeditions found areas where, alarmingly, 50 per cent of the fish had them.

"I asked a NOAA [National Oceanic and Atmospheric Administration] sampler what percentage of fish they find with sores prior to 2010, and it's one tenth of one percent," Cowan said. "Which is what we found prior to 2010 as well. But nothing like we've seen with these secondary infections and at this high of rate since the spill."

"What we think is that it's attributable to chronic exposure to PAHs released in the process of weathering of oil on the seafloor," Cowan said. "There's no other thing we can use to explain this phenomenon. We've never seen anything like this before."

Official response

Questions raised by Al Jazeera's investigation remain largely unanswered.

Al Jazeera contacted the office of Louisiana governor Bobby Jindal, who provided a statement that said the state continues to test its waters for oil and dispersants, and that it is testing for PAHs.

"Gulf seafood has consistently tested lower than the safety thresholds established by the FDA for the levels of oil and dispersant contamination that would pose a risk to human health," the statement reads. "Louisiana seafood continues to go through extensive testing to ensure that seafood is safe for human consumption. More than 3,000 composite samples of seafood, sediment and water have been tested in Louisiana since the start of the spill."

Signs of the impact on the regional ecosystem are ominous: mutated shrimp, fish with oozing sores, underdeveloped blue crabs lacking claws, eyeless crabs and shrimp - and scientists and fishermen point fingers towards BP's oil as being the cause [Keath Ladner]

At the federal government level, the Food and Drug Administration and Environmental Protection Agency - both federal agencies which have powers in the this area - insisted Al Jazeera talk with the National Oceanic and Atmospheric Administration (NOAA). 

NOAA won't comment to the media because its involvement in collecting information for an ongoing lawsuit against BP.

BP refused Al Jazeera's request to comment on this issue for a television interview, but provided a statement that read:

"Seafood from the Gulf of Mexico is among the most tested in the world, and, according to the FDA and NOAA, it is as safe now as it was before the accident."

BP claims that fish lesions are common, and that prior to the Deepwater Horizon accident there was documented evidence of lesions in the Gulf of Mexico caused by parasites and other agents.

The oil giant added: 

"As part of the Natural Resource Damage Assessment, which is led by state and federal trustees, we are investigating the extent of injury to natural resources due to the accident".

"BP is funding multiple lines of scientific investigation to evaluate potential damage to fish, and these include: extensive seafood testing programs by the Gulf states; fish population monitoring conducted by the Louisiana Department of Wildlife and Fisheries, Auburn University and others; habitat and water quality monitoring by NOAA; and toxicity tests on regional species. The state and federal Trustees will complete an injury assessment and the need for environmental restoration will be determined."

Before and after

But evidence of ongoing contamination continues to mount.

Crustacean biologist Darryl Felder, in the Department of Biology with the University of Louisiana at Lafayette is in a unique position.

Felder has been monitoring the vicinity of BP's blowout Macondo well both before and after the oil disaster began, because, as he told Al Jazeera, "the National Science Foundation was interested in these areas that are vulnerable due to all the drilling".

"So we have before and after samples to compare to," he added. "We have found seafood with lesions, missing appendages, and other abnormalities."

Felder also has samples of inshore crabs with lesions. "Right here in Grand Isle we see lesions that are eroding down through their shell. We just got these samples last Thursday and are studying them now, because we have no idea what else to link this to as far as a natural event."

According to Felder, there is an even higher incidence of shell disease with crabs in deeper waters.

"My fear is that these prior incidents of lesions might be traceable to microbes, and my questions are, did we alter microbial populations in the vicinity of the well by introducing this massive amount of petroleum and in so doing cause microbes to attack things other than oil?"

One hypothesis he has is that the waxy coatings around crab shells are being impaired by anthropogenic chemicals or microbes resulting from such chemicals.

"You create a site where a lesion can occur, and microbes attack. We see them with big black lesions, around where their appendages fall off, and all that is left is a big black ring."

Felder added that his team is continuing to document the incidents: "And from what we can tell, there is a far higher incidence we're finding after the spill."

"We are also seeing much lower diversity of crustaceans," he said. "We don't have the same number of species as we did before [the spill]."

[Continues below the slideshow]

On April 20, 2010, the United States experienced the beginning of the country's largest environmental disaster in its history, when the Deepwater Horizon oil rig exploded and sank, flooding the Gulf of Mexico with at least 4.9 million barrels of crude oil over an 87-day period. Erika Blumenfeld/Al Jazeera

Compounding the devastating effects of the oil itself, were at least 1.9m gallons of toxic chemicals and industrial solvents which where poured into the ocean in an attempt to disperse the oil.

Erika Blumenfeld/Al Jazeera

Many of these chemicals, such as the petroleum distillates and especially 2-butoxyethanol, are medically known to be teratogenic, mutagenic, and carcinogenic, and exposure to them can lead to a long list of serious health effects, including death.

Erika Blumenfeld/Al Jazeera

Marine and wildlife throughout the region were exposed to the oil and dispersants, resulting in mass deaths of many species including turtles, dolphins, birds, fish and crustaceans

Erika Blumenfeld/Al Jazeera

Fishermen and women along the Gulf Coast are telling of record low seasonal harvests of shrimp, oysters, and fish, with many of the coastal leases yielding 75-90 percent less than normal.

Erika Blumenfeld/Al Jazeera

Keath Ladner, a third generation seafood processor in Hancock County, Mississippi, told Al Jazeera that the brown shrimp catch has dropped by two-thirds, and that the white shrimp have been wiped out.

Erika Blumenfeld/Al Jazeera

Most commercial fishing areas in the oil disaster effected areas are open to commercial fishing, and the state and federal governments have declared that the seafood is safe and is not testing positive to the toxic oil and dispersant chemicals.

Erika Blumenfeld/Al Jazeera

Tracy Khuns and Mike Roberts, commercial fishers from Barataria Bay, Louisiana, have been finding eyeless shrimp and other seafood deformities in their waters, and believe the cause to be chemicals from BP's oil and dispersants.

Erika Blumenfeld/Al Jazeera

Kuhn's told Al Jazeera that in September 2011 their friend caught 400 pounds of eyeless white shrimp, and said that at least 50 per cent of the shrimp caught in that period in Barataria Bay, an area heavily impacted by BP's oil and dispersants, were eyeless.

Erika Blumenfeld/Al Jazeera

When asked to comment on the allegations that scientists and fishermen are saying about deformed seafood and low populations, BP provided Al Jazeera with this statement: "Seafood from the Gulf of Mexico is among the most tested in the world, and according to the FDA and NOAA, it is as safe now as it was before the accident."

Erika Blumenfeld/Al Jazeera

Jonathan Henderson of Gulf Restoration Network, continues to find tar balls along the beaches and oil in the marshes of Louisiana. Al Jazeera recently documented massive submerged tar mats being excavated by BP clean up crews.

Erika Blumenfeld/Al Jazeera

There continue to be unexplained mass deaths of many species along the coast, from dolphins to birds. Gulf Coast residents and scientists are concerned for the future and the health of their ecosystems and the food chain.

Erika Blumenfeld/Al Jazeera

Felder has tested his samples for oil, but not found many cases where hydrocarbon traces tested positive. Instead, he believes what he is seeing in the deepwater around BP's well is caused from the "huge amount" of drilling mud used during the effort to stop the gushing well.

"I was collecting deepwater shrimp with lesions on the side of their carapace. Under the lesions, the gills were black. The organ that propels the water through the gills, it too was jet-black. That impairs respiratory ability, and has a negative effect on them. It wasn't hydrocarbons, but is largely manganese precipitates, which is really odd. There was a tremendous amount of drilling mud pumped out with Macondo, so this could be a link."

Some drilling mud and oil well cement slurries used on oil extraction rigs contains up to 90 per cent by weight of manganomanganic (manganese) oxide particles.

Felder is also finding "odd staining" of animals that burrow into the mud that cause stain rings, and said: "It is consistently mineral deposits, possibly from microbial populations in [overly] high concentrations."

A direct link

Dr Andrew Whitehead, an associate professor of biology at Louisiana State University, co-authored the report Genomic and physiological footprint of the Deepwater Horizon oil spill on resident marsh fishes that was published in the journal Proceedings of the National Academy of Sciences in October 2011.

Whitehead's work is of critical importance, as it shows a direct link between BP's oil and the negative impacts on the Gulf's food web evidenced by studies on killifish before, during and after the oil disaster.

"What we found is a very clear, genome-wide signal, a very clear signal of exposure to the toxic components of oil that coincided with the timing and the locations of the oil," Whitehead told Al Jazeera during an interview in his lab.

According to Whitehead, the killifish is an important indicator species because they are the most abundant fish in the marshes, and are known to be the most important forage animal in their communities.

"That means that most of the large fish that we like to eat and that these are important fisheries for, actually feed on the killifish," he explained. "So if there were to be a big impact on those animals, then there would probably be a cascading effect throughout the food web. I can't think of a worse animal to knock out of the food chain than the killifish."

But we may well be witnessing the beginnings of this worst-case scenario.

Whitehead is predicting that there could be reproductive impacts on the fish, and since the killifish is a "keystone" species in the food web of the marsh, "Impacts on those species are more than likely going to propagate out and effect other species. What this shows is a very direct link from exposure to DWH oil and a clear biological effect. And a clear biological effect that could translate to population level long-term consequences."

Back on shore, troubled by what he had been seeing, Keath Ladner met with officials from the US Food and Drug Administration and asked them to promise that the government would protect him from litigation if someone was made sick from eating his seafood.

"They wouldn't do it," he said.

"I'm worried about the entire seafood industry of the Gulf being on the way out," he added grimly.

'Tar balls in their crab traps'

Ed Cake, a biological oceanographer, as well as a marine and oyster biologist, has "great concern" about the hundreds of dolphin deaths he has seen in the region since BP's disaster began, which he feels are likely directly related to the BP oil disaster.

"Adult dolphins' systems are picking up whatever is in the system out there, and we know the oil is out there and working its way up the food chain through the food web - and dolphins are at the top of that food chain."

Cake explained: "The chemicals then move into their lipids, fat, and then when they are pregnant, their young rely on this fat, and so it's no wonder dolphins are having developmental issues and still births."

Cake, who lives in Mississippi, added: "It has been more than 33 years since the 1979 Ixtoc-1 oil disaster in Mexico's Bay of Campeche, and the oysters, clams, and mangrove forests have still not recovered in their oiled habitats in seaside estuaries of the Yucatan Peninsula. It has been 23 years since the 1989 Exxon Valdez oil disaster in Alaska, and the herring fishery that failed in the wake of that disaster has still not returned."

Cake believes we are still in the short-term impact stage of BP's oil disaster.

"I will not be alive to see the Gulf of Mexico recover," said Cake, who is 72 years old. "Without funding and serious commitment, these things will not come back to pre-April 2010 levels for decades."

The physical signs of the disaster continue.

"We're continuing to pull up oil in our nets," Rooks said. "Think about losing everything that makes you happy, because that is exactly what happens when someone spills oil and sprays dispersants on it. People who live here know better than to swim in or eat what comes out of our waters."

Khuns and her husband told Al Jazeera that fishermen continue to regularly find tar balls in their crab traps, and hundreds of pounds of tar balls continue to be found on beaches across the region on a daily basis.

Meanwhile Cowan continues his work, and remains concerned about what he is finding.

"We've also seen a decrease in biodiversity in fisheries in certain areas. We believe we are now seeing another outbreak of incidence increasing, and this makes sense, since waters are starting to warm again, so bacterial infections are really starting to take off again. We think this is a problem that will persist for as long as the oil is stored on the seafloor."

Felder wants to continue his studies, but now is up against insufficient funding.

Regarding his funding, Cowan told Al Jazeera: "We are up against social and economic challenges that hamper our ability to get our information out, so the politics have been as daunting as the problem [we are studying] itself. But my funding is not coming from a source that requires me to be quiet."

Follow Dahr Jamail on Twitter: @DahrJamail

Read more about the scientists in this article, and their findings:

Dr Darryl Felder, Department of Biology, University of Louisiana, Lafayette. Runs a research lab that studies the biology of marine crustaceans. Dr Felder has been monitoring the seafloor in the vicinity of BP's blow-out Macondo oil-well both before and after the oil disaster began. He was studying samples from the seafloor in the Macondo area pre-spill via funding from the National Science Foundation, which provided him a grant to log the effects of all the drilling in the area. His funding now comes from the Gulf Research Initiative (GRI), which is funded by BP. Read his full biography here.

Dr Jim Cowan with Louisiana State University's Department of Oceanography and Coastal Sciences has been studying Gulf seafood, specifically red snapper, for more than 20 years. Funding is primarily via LSU, although LSU has also received funding via GRI. Read his full biography here.

Dr Andrew Whitehead, LSU, his lab conducts experiments and studies on Evolutionary and Ecological Genomics. He recently published "Genomic and physiological footprint of the Deepwater Horizon oil spill on resident marsh fishes" in the National Academy of Sciences. Much of his funding also comes from the Gulf Research Initiative. Read his full biography here.

Brief summary of scientists' findings/studies:

Felder: Studies carried out from January 2010 to present in BP's Macondo well area. Found abnormalities in shrimp post-spill, whereas pre-spill found none.

Cowan: Studies carried out from Nov 2010-present, from west Louisiana to west Florida, from coast to 250km out. Found lesions/sores/infections in 20 species of fish, as many as 50 per cent fish in some samples impacted. Pre spill levels were 1/10 of one per cent of fish.

Whitehead: Species such as the Gulf Killifish, in and around the Gulf of Mexico, will continue to be subject to negative effects of the BP oil spill disaster of 2010. The Killifish, which researchers consider a good indicator of water quality in the Gulf of Mexico, is showing signs that the oil spill is having a negative impact on its health. Tracked killifish for the first four months after spill across oil-impacted areas of Louisiana and Mississippi.