Ángela Restrepo Moreno: "La mamá de los científicos"

INVESTIGADORES EMÉRITOS 2014

Ángela Restrepo, ganadora en la categoría ciencias Bio - de la Vida y el Medio Ambiente.

De niña, Ángela Restrepo Moreno se quedaba por horas mirando la vitrina de la farmacia de su abuelo, detrás de la cual había un aparato de color amarillo con negro que la atraía como si fuera un imán. Era un microscopio muy parecido al que usaba Louis Pasteur en el siglo XIX para sus estudios.

Esto llevó a esta valiente mujer a ser científica en una época en la que las mujeres solo tenían dos caminos posibles: ser monjas o amas de casa. Cuando Ángela se graduó de bachiller, en 1951, no había dónde estudiar microbiología en Medellín. Su panorama se esclareció cuando abrieron un curso de Bacteriología. Luego hizo un máster en la Universidad de Tulane, en Estados Unidos. Años después hizo el doctorado y a su regreso comenzó a hacer diagnósticos de enfermedades causadas por hongos y microbios en un cuartico que el Hospital Pablo Tobón Uribe le prestó a ella y a otros investigadores. Gracias al trabajo de estos científicos y a do-naciones hoy es un edificio de cuatro plantas que todos conocen como la Corporación para Investigaciones Biológicas. Ángela Restrepo es hoy por hoy una autoridad mundial en el estudio del hongo Paracoccidioides brasiliensis.

Por su trabajo Ángela Restrepo ha sido reconocida con una larga lista de condecoraciones. Hace 20 años integró la Misión de Sabios que, junto con el educador Carlos E. Vasco, el escritor Gabriel García Márquez y el científico Rodolfo Llinás, le propuso al país una ruta de educación para catapultarlo hacia el desarrollo.

La doctora Restrepo es reconocida por haber sembrado la semilla de la investigación en una veintena de médicos y microbiólogos que hoy tienen estudios de doctorado y que la consideran como su mamá, tanto en la ciencia como en la vida. “Nunca me angustié de ser una mujer soltera por la multiplicación de los científicos que he visto crecer a mi lado”, dice ella.

ORIGINAL: Semana
05 julio 2014 

Meet the electric life forms that live on pure energy

Photo credit: Shewanella oneidensis / U.S. Department of Energy

Unlike any other life on Earth, these extraordinary bacteria use energy in its purest form – they eat and breathe electrons – and they are everywhere

STICK an electrode in the ground, pump electrons down it, and they will come: living cells that eat electricity. We have known bacteria to survive on a variety of energy sources, but none as weird as this. Think of Frankenstein's monster, brought to life by galvanic energy, except these "electric bacteria" are very real and are popping up all over the place.

Unlike any other living thing on Earth, electric bacteria use energy in its purest form – naked electricity in the shape of electrons harvested from rocks and metals. We already knew about two types, Shewanella and Geobacter. Now, biologists are showing that they can entice many more out of rocks and marine mud by tempting them with a bit of electrical juice. Experiments growing bacteria on battery electrodes demonstrate that these novel, mind-boggling forms of life are essentially eating and excreting electricity.

That should not come as a complete surprise, says Kenneth Nealson at the University of Southern California, Los Angeles. We know that life, when you boil it right down, is a flow of electrons: "You eat sugars that have excess electrons, and you breathe in oxygen that willingly takes them." Our cells break down the sugars, and the electrons flow through them in a complex set of chemical reactions until they are passed on to electron-hungry oxygen.

In the process, cells make ATP, a molecule that acts as an energy storage unit for almost all living things. Moving electrons around is a key part of making ATP. "Life's very clever," says Nealson. "It figures out how to suck electrons out of everything we eat and keep them under control." In most living things, the body packages the electrons up into molecules that can safely carry them through the cells until they are dumped on to oxygen.

"That's the way we make all our energy and it's the same for every organism on this planet," says Nealson. "Electrons must flow in order for energy to be gained. This is why when someone suffocates another person they are dead within minutes. You have stopped the supply of oxygen, so the electrons can no longer flow."


The discovery of electric bacteria shows that some very basic forms of life can do away with sugary middlemen and handle the energy in its purest form – electrons, harvested from the surface of minerals. "It is truly foreign, you know," says Nealson. "In a sense, alien."

Nealson's team is one of a handful that is now growing these bacteria directly on electrodes, keeping them alive with electricity and nothing else – neither sugars nor any other kind of nutrient. The highly dangerous equivalent in humans, he says, would be for us to power up by shoving our fingers in a DC electrical socket.

To grow these bacteria, the team collects sediment from the seabed, brings it back to the lab, and inserts electrodes into it.

First they measure the natural voltage across the sediment, before applying a slightly different one. A slightly higher voltage offers an excess of electrons; a slightly lower voltage means the electrode will readily accept electrons from anything willing to pass them off. Bugs in the sediments can either "eat" electrons from the higher voltage, or "breathe" electrons on to the lower-voltage electrode, generating a current. That current is picked up by the researchers as a signal of the type of life they have captured.

"Basically, the idea is to take sediment, stick electrodes inside and then ask 'OK, who likes this?'," says Nealson.

Shocking breath

At the Goldschmidt geoscience conference in Sacramento, California, last month, Shiue-lin Li of Nealson's lab presented results of experiments growing electricity breathers in sediment collected from Santa Catalina harbour in California. Yamini Jangir, also from the University of Southern California, presented separate experiments which grew electricity breathers collected from a well in Death Valley in the Mojave Desert in California.

Over at the University of Minnesota in St Paul, Daniel Bond and his colleagues have published experiments showing that they could grow a type of bacteria that harvested electrons from an iron electrode (mBio, doi.org/tqg). That research, says Jangir's supervisor Moh El-Naggar, may be the most convincing example we have so far of electricity eaters grown on a supply of electrons with no added food.

But Nealson says there is much more to come. His PhD student Annette Rowe has identified up to eight different kinds of bacteria that consume electricity. Those results are being submitted for publication.


Nealson is particularly excited that Rowe has found so many types of electric bacteria, all very different to one another, and none of them anything like Shewanella or Geobacter. "This is huge. What it means is that there's a whole part of the microbial world that we don't know about."

Discovering this hidden biosphere is precisely why Jangir and El-Naggar want to cultivate electric bacteria. "We're using electrodes to mimic their interactions," says El-Naggar. "Culturing the 'unculturables', if you will." The researchers plan to install a battery inside a gold mine in South Dakota to see what they can find living down there.

NASA is also interested in things that live deep underground because such organisms often survive on very little energy and they may suggest modes of life in other parts of the solar system.

Electric bacteria could have practical uses here on Earth, however, such as creating biomachines that do useful things like clean up sewage or contaminated groundwater while drawing their own power from their surroundings. Nealson calls them self-powered useful devices, or SPUDs.

Practicality aside, another exciting prospect is to use electric bacteria to probe fundamental questions about life, such as what is the bare minimum of energy needed to maintain life.

For that we need the next stage of experiments, says Yuri Gorby, a microbiologist at the Rensselaer Polytechnic Institute in Troy, New York: bacteria should be grown not on a single electrode but between two. These bacteria would effectively eat electrons from one electrode, use them as a source of energy, and discard them on to the other electrode.

Gorby believes bacterial cells that both eat and breathe electrons will soon be discovered. "An electric bacterium grown between two electrodes could maintain itself virtually forever," says Gorby. "If nothing is going to eat it or destroy it then, theoretically, we should be able to maintain that organism indefinitely."

It may also be possible to vary the voltage applied to the electrodes, putting the energetic squeeze on cells to the point at which they are just doing the absolute minimum to stay alive. In this state, the cells may not be able to reproduce or grow, but they would still be able to run repairs on cell machinery. "For them, the work that energy does would be maintaining life – maintaining viability," says Gorby.

How much juice do you need to keep a living electric bacterium going? Answer that question, and you've answered one of the most fundamental existential questions there is.

This article appeared in print under the headline "The electricity eaters"

Leader: "Spark of life revisited thanks to electric bacteria"

Wire in the mud

Electric bacteria come in all shapes and sizes. A few years ago, biologists discovered that some produce hair-like filaments that act as wires, ferrying electrons back and forth between the cells and their wider environment. They dubbed them microbial nanowires.

Lars Peter Nielsen and his colleagues at Aarhus University in Denmark have found that tens of thousands of electric bacteria can join together to form daisy chains that carry electrons over several centimetres – a huge distance for a bacterium only 3 or 4 micrometres long. It means that bacteria living in, say, seabed mud where no oxygen penetrates, can access oxygen dissolved in the seawater simply by holding hands with their friends.

Such bacteria are showing up everywhere we look, says Nielsen. One way to find out if you're in the presence of these electron munchers is to put clumps of dirt in a shallow dish full of water, and gently swirl it. The dirt should fall apart. If it doesn't, it's likely that cables made of bacteria are holding it together.

Nielsen can spot the glimmer of the cables when he pulls soil apart and holds it up to sunlight (see video). 

Flexible biocables

It's more than just a bit of fun. Early work shows that such cables conduct electricity about as well as the wires that connect your toaster to the mains. That could open up interesting research avenues involving flexible, lab-grown biocables.

ORIGINAL: New Scientist
by Catherine Brahic
16 July 2014

The Forgotten Woman Who Made Microbiology Possible

Angelina Fanny Hesse: An Unsung Heroine of Microbiology
Collage by Fruzsina Eördögh; Petri dish image © M J Richardson (CC BY-SA 2.0)

Lab work can be a lot like cooking. You have to follow directions to measure, mix, and heat different chemicals to the right temperature to get the desired result. For some experiments, the desired result is actually something that can be eaten by a range of different organisms. In microbiology labs, feeding bacteria is a major preoccupation, and preparing the proper growth medium in a lab's "kitchen" is often the first step of any experiment. Petri dishes are filled with a sort of savory Jell-O, a nutrient-filled semi-solid matrix that creates a cozy home for bacteria to grow. Without the solid-yet-moist surface of the gel where the bacteria can cling to and reproduce, there's little hope of separating a bacterial cell from its environment in order to study it.

In the earliest days of microbiology, scientists were stumped about how to isolate bacteria. That is, until the family cook—a woman named Angelina—changed everything by bringing her culinary insight into the lab. Before Angelina, the work of classifying different bacteria seemed hopelessly complex. Unable to differentiate them, Linnaeus classified all bacteria in the order Chaos in 1763. (Today, Chaos is a genus of giant amoebae.) In the 1800s, scientists studying the spots of fungus growing on moldy bread and meat began to realize that each spot was an individual species of microorganism, which could be transferred to a fresh piece of food and grown in isolation. Inspired by these early food-based studies, Robert Koch used thin slices of potatoes as naturally occurring "Petri dishes" when he began his studies of bacterial pathogens.

New techniques to isolate, grow, and study the behavior of individual species of microorganisms were developed in Koch's lab in the last decades of the 19th century. In a 1939 article, Arthur Hitchens and Morris Leikind described the history of these crucial microbiological techniques and the development of the solid medium still used in labs today. They begin by writing that Robert Koch's "genius lay in his ability to bring order out of chaos. Starting as it were with a box of miscellaneous beads, varying in size and shape, each bead a scientific fact, he found a thread on which the beads could be strung to form a perfect necklace." But they continue to highlight not only the genius "bead stringers" but also the numerous and talented "bead collectors" who help to build the tools and collect the data that the bead stringers use. For Koch's legendary discoveries of the bacteria that cause diseases like tuberculosis and cholera to be possible, he needed new techniques to effectively isolate bacteria beyond carefully sliced potatoes. He needed the tools that were developed by his less-celebrated laboratory assistants, like Julius Richard Petri's dishes and Walther Hesse's solid growth medium.

But behind the talented laboratory technicians that supported Robert Koch's genius was an even more unsung heroine of microbiology. It was Walther Hesse's wife (who was often an assistant and scientific illustrator for the lab) Angelina Fanny Hesse who made the isolation of bacteria possible. In the early 1880's, Walther was struggling to find the right sort of gel for Petri's dishes. He was experimenting with using gelatin to congeal the nutrient broth that the bacteria ate, but bacteria also liked to eat the proteins that congealed the gelatin, chewing through the gel and ruining the experiments. Gelatin also had another major drawback: it would soften and begin to melt at the incubation temperatures required for growing the bacteria.

Angelina, who cooked both the family's meals and the beef stock that the bacteria ate in her kitchen, suggested that Walther use agar-agar, which is more heat-stable than gelatin and used to make soups, desserts, and jellies, particularly in Asia. (She had learned about it from Dutch friends who had lived in Indonesia, which was a colony of the Netherlands at the time.) Agar is a sugar polymer derived from algae that most bacteria can't digest. Once it's boiled and cooled, it forms a tough matrix that stays solid at much higher temperatures than gelatin.

With agar, many of the technical problems hindering Hesse's—and therefore Koch's—experimental progress were solved. Koch briefly mentioned the development (though he fails to mention either Walther or Angelina) in his 1882 paper announcing the identification of the bacteria that causes tuberculosis: "The tubercule bacilli can also be cultivated on other media...they grow, for example, on a gelatinous mass which was prepared with agar-agar, which remains solid at blood temperature, and which has received a supplement of meat broth and peptone."

Angelina Hesse's creative insight was thus written out of history with the ever-present passive voice of the scientific literature. Even today, the Wikipedia article about Robert Koch masks Angelina's contribution to microbiological history, simply stating that Koch "began to utilize agar to grow and isolate pure cultures." In the late 19th century, the use of agar to isolate bacteria was initially referred to as "Koch's plate technique," but since the early 1900s only Petri's name remains in common use. In their article, Hitchens and Leikind suggested (seventy five years ago) that "plain agar" be referred to as "Frau Hesse's medium" to acknowledge her forgotten "service to science and to humanity." Perhaps it's finally time that we remember Frau Hesse and celebrate all the ignored "bead collectors"

ORIGINAL: Popular Science

By Christina Agapakis
Posted 07.14.2014

South America's Hidden Epidemic

Richard Arboleda. Test subject. A Colombian boy gets a breath test for H. pylori.

The Spanish Conquest brought smallpox and measles epidemics that decimated the peoples of the New World. But another pathogen arrived with the colonists, the bacterium called Helicobacter pylori, and new research may explain why it has quietly wreaked havoc in the stomachs of some in the Americas ever since.

More than half of all humans carry H. pylori, and the microbe seems to protect against childhood asthma and esophageal cancer. Yet it causes stomach ulcers and is responsible for 80% to 90% of all stomach cancers, making it the world's second leading cause of cancer mortality, after tobacco. Not everyone harboring the microbe develops stomach cancer, however; in certain parts of the world—much of Africa, for example—such cancers are rare even though many people harbor H. pylori. Microbiologists call this “the African enigma.”

So, why are some hit much harder than others by H. pylori? A group led by researchers at Vanderbilt University in Nashville has been exploring that question in Colombia. The team had previously found that stomach cancer rates in Túquerres, a mountain town in the Andes, were about 150/100,000, compared with 6/100,000 in Tumaco, a coastal city.

In the new study, the team conducted genetic analyses of 121 people from each town who had sought medical attention for stomach pain. The study confirmed that the DNA of the coastal people was largely of African origin; the mountain group, on the other hand, was on average two-thirds Amerindian and a third European, with small traces of African DNA.

The researchers also examined the DNA of the H. pylori specimens collected from the 242 individuals. The bacterium, which has colonized humans for more than 60,000 years, has evolved into distinct strains reflecting its history, such as whether it came from Europe or Africa. Both coastal and mountain groups were colonized with H. pylori strains that had DNA segments of both African and European origin.

Whether they lived in the mountains or the coast, the people of Amerindian descent carrying largely African strains of H. pylori were five times more likely to have gastric cancer or precancerous lesions than were people of largely African descent who carried similar strains, the group reports online today in the Proceedings of the National Academy of Sciences.

Scientists had not previously examined the role that coevolution of host and organism might play in the H. pylori-connected stomach cancer. “We looked at both the bug and the people infected with it,” says study co-author Barbara Schneider, a Vanderbilt molecular biologist. “It turns out that African ancestry in H. pylori strains, combined with Native American ancestry in humans, is a bad combination.”

Those in Tumaco, however, may enjoy their relative protection against stomach cancer because their African ancestors, on the other hand, apparently coevolved with their strains of H. pylori in ways that minimized the carcinogenic effects.

The researchers don't know why people of Amerindian descent are more susceptible to the African H. pylori sequences. Some H. pylori strains contain a set of genes that create a needlelike structure that deposits a cancerous protein called CagA into human cells. These strains are especially carcinogenic. In the Vanderbilt study, however, the impact of combined Amerindian host ancestry and African H. pylori ancestry was five times stronger than that of being infected with a strain that has the CagA-associated genes. One H. pylori interaction may be with diet. The coastal people eat more fresh fruits and vegetables and fish than the more cancer-prone residents of the Andes.

The findings could help fight stomach cancer by offering a way to determine who is at risk from H. pylori infection. More at-risk people could be treated with antibiotics or monitored for gastric lesions that may lead to cancer.

“H. pylori is mostly harmless but it can be deadly,” says infectious disease specialist Jay Solnick of the University of California, Davis, who was not involved in the research. “We've been looking for many years for biomarkers of who should be treated or screened intensively. This could help.”

ORIGINAL: Science Magazine
13 January 2014

Biggest Virus Yet Found, May Be Fourth Domain of Life?

ORIGINAL: NatGeo

Christine Dell'Amor. National Geographic
July 18, 2013

Pandoraviruses opening up new questions about life as we know it.

An image of a Pandoravirus particle, created using an electron microscope.
Image courtesy Chantal Abergel and Jean-Michel Claverie

Scientists have found the biggest viruses known, and these pandoraviruses have opened up entirely new questions in science—even suggesting a fourth domain of life, a new study says.

Each about one micron—a thousandth of a millimeter—in length, the newfound genus Pandoravirus dwarfs other viruses, which range in size from about 50 nanometers up to 100 nanometers. A genus is a taxonomic ranking between species and family.

In addition to being huge, pandoraviruses have supersize DNA: 2,500 genes as compared with 10 genes in many viruses. (Get a genetics overview.)

Microbiology was similarly upturned about ten years ago when scientists found the genus Mimivirus—the first large virus of its kind at about 0.7 micron.

Following the discovery of Mimivirus and an even larger behemoth called Megavirus chilensis, "we have been thinking deeply into the limits of viruses, and this is why we're open more than other labs to finding exotic things—we push the envelope of what we would consider possible," said study co-author Jean-Michel Claverie, a microbiologist at Aix-Marseille Université in France, who is part of a research team with microbiologist Chantal Abergel.

So the pair and their colleagues began hunting for more giant viruses in water sediments, where other big viruses have been found due to the abundance of amoeba prey.

Sure enough, they found two: Pandoravirus salinus, from the mouth of Chile's Tunquen River, and Pandoravirus dulcis from a freshwater pond near Melbourne, Australia—both of which parasitize amoebas. (Also see "Virus-Infecting Virus Fuels Definition of Life Debate.")

"Finding such a new type of virus that is so different happens once every 50 years—it's a major discovery," said the team, whose study appears today in the journal Science.

Why haven't scientists found pandoraviruses before?

There are several reasons, but a simple one is that many scientists still assume viruses are small.

"When people look into cells and when they see things that don't have the right dimension or don't have regular assets or geometries, they don't think of viruses—they think its some kind of bacteria," Claverie and Abergel said.

When the scientists then try to cultivate these supposed bacteria in the laboratory and fail, it doesn't surprise them, since up to 60 percent of bacteria in the oceans can't be grown in the lab.

The study authors also note that Pandoravirus may had already been found 13 years ago—but scientists just didn't know what it was. (See more pictures of viruses.)

When the team screened scientific literature on parasites that eat a type of amoeba called Acanthamoeba, they found mention of Pandoravirus-like particles.

How are pandoraviruses different than other viruses?

Simply put, they have little in common with other viruses—"something that came as a surprise to us," the team said.

For one, the virus reproduces in a curious fashion. Most viruses start a new cell by building an empty "box" and filling it up with DNA over time. But curiously, pandoraviruses do both of these processes at the same time in a process the team calls "knitting." (Read blog post: "An Infinity of Viruses.")

Perhaps most striking, 93 percent of pandoraviruses' 2,500 genes cannot be traced back to any known lineage in nature. In other words, they are completely alien to us.

Such foreign genes, the team suggests, is evidence for the "controversial existence of a fourth domain of life," in addition to bacteria, archaea, and eukaryota, the latter of which includes complex life like us.

The three-domain system is "probably pretty wrong—we are missing some part of the puzzle here," the team said.

What should you know about these viruses?

First and foremost, that they're not harmful to people, the team emphasized: Most viruses infect other microbes.

In fact, many pandoraviruses and similar marine viruses may have a beneficial—and unseen—role in nature. (See National Geographic's pictures of marine microbes.)

For instance, viruses prey on and thus regulate a lot of the ocean's phytoplankton, which produces half of our planet's oxygen and forms the base of the ocean's food chain.

Overall, the team added, the discovery of pandoraviruses "demonstrates our shallow knowledge of microbiology on Earth."

Follow Christine Dell'Amore on Twitter and Google .

Cells as living calculators

ORIGINAL: MIT

Anne Trafton, MIT News Office

May 15, 2013

Using analog computation circuits, MIT engineers design cells that can compute logarithms, divide and take square roots.

MIT engineers have created synthetic biology circuits that can perform analog computations such as taking logarithms and square roots in living cells. ILLUSTRATION COURTESY OF THE RESEARCHERS

MIT engineers have transformed bacterial cells into living calculators that can compute logarithms, divide, and take square roots, using three or fewer genetic parts.

Inspired by how analog electronic circuits function, the researchers created synthetic computation circuits by combining existing genetic “parts,” or engineered genes, in novel ways.

The circuits perform those calculations in an analog fashion by exploiting natural biochemical functions that are already present in the cell rather than by reinventing them with digital logic, thus making them more efficient than the digital circuits pursued by most synthetic biologists, according to Rahul Sarpeshkar and Timothy Lu, the two senior authors on the paper, describing the circuits in the May 15 online edition of Nature.

“In analog you compute on a continuous set of numbers, which means it’s not just black and white, it’s gray as well,” says Sarpeshkar, an associate professor of electrical engineering and computer science and the head of the Analog Circuits and Biological Systems group at MIT

Analog computation would be particularly useful for designing cellular sensors for pathogens or other molecules, the researchers say. Analog sensing could also be combined with digital circuits to create cells that can take a specific action triggered by a threshold concentration of certain molecules.

“You could do a lot of upfront sensing with the analog circuits because they’re very rich and a relatively small amount of parts can give you a lot of complexity, and have that output go into a circuit that makes a decision — is this true or not?” says Lu, an assistant professor of electrical engineering and computer science and biological engineering. 

Lead author of the Nature paper is MIT postdoc Ramiz DanielJacob Rubens, a graduate student in microbiology, is also an author of the paper.

Analog advantages 

Sarpeshkar has previously identified thermodynamic similarities between analog transistor circuits and the chemical circuits that take place inside cells. In 2011, he took advantage of those similarities to model biological interactions between DNA and proteins in an electronic circuit, using only eight transistors. 

In the new Nature paper, Sarpeshkar, Lu and colleagues have done the reverse — mapping analog electronic circuits onto cells. Sarpeshkar has long advocated analog computing as a more efficient alternative to digital computation at the moderate precision of computation seen in biology. These analog circuits are efficient because they can take in a continuous range of inputs, and they exploit the natural continuous computing functions that are already present in cells. In the case of cells, that continuous input might be the amount of glucose present. In transistors, it’s a range of continuous input currents or voltages.

Digital circuits, meanwhile, represent every value as zero or one, ignoring the range of possibilities in between. This can be useful for creating circuits that perform logic functions such as AND, NOT and OR inside cells, which many synthetic biologists have done. These circuits can reveal whether or not a threshold level of a certain molecule is present, but not the exact amount of it.

Digital circuits also require many more parts, which can drain the energy of the cell hosting them. “If you build too many parts to make some function, the cell is not going to have the energy to keep making those proteins,” Sarpeshkar says.

Doing the math

To create an analog adding or multiplying circuit that can calculate the total quantity of two or more compounds in a cell, the researchers combined two circuits, each of which responds to a different input. In one circuit, a sugar called arabinose turns on a transcription factor that activates the gene that codes for green fluorescent protein (GFP). In the second, a signaling molecule known as AHL also turns on a gene that produces GFP. By measuring the total amount of GFP, the total amount of both inputs can be calculated. 

To subtract or divide, the researchers swapped one of the activator transcription factors with a repressor, which turns off production of GFP when the input molecule is present. The team also built an analog square root circuit that requires just two parts, while a recently reported digital synthetic circuit for performing square roots had more than 100.

“Analog computation is very efficient,” Sarpeshkar says. “To create digital circuits at a comparable level of precision would take many more genetic parts.”

Another of the team’s circuits can perform division by calculating the ratio of two different molecules. Cells often perform this kind of computation on their own, which is critical for monitoring the relative concentrations of molecules such as NAD and NADH, which are frequently converted from one to the other as they help other cellular reactions take place.

“That ratio is important for controlling a lot of cellular processes, and the cell naturally has enzymes that can recognize those ratios,” Lu says. “Cells can already do a lot of these things on their own, but for them to do it over a useful range requires extra engineering.”

That extra engineering included modifying the circuits so that they can compute with inputs over a range of 1 to 10,000 — much wider than the range of a naturally occurring cell circuit. 

“It’s nice to see that frameworks from electrical engineering can be concisely and elegantly mapped into synthetic biology,” says Eric Klavins, an associate professor of electrical engineering and adjunct associate professor of biological engineering at the University of Washington who was not part of the research team.

The researchers are now trying to create analog circuits in nonbacterial cells, including mammalian cells. They are also working on expanding the library of genetic parts that can be incorporated into the circuits. “Right now we’re using three of the most commonly used transcription factors in biology, but we’d like to do this with additional parts and make this a generalizable platform so everyone else can use it,” Lu says.

“We have just scratched the surface of what sophisticated analog feedback circuits can do in living cells,” says Sarpeshkar, whose lab is working on building further new analog circuits in cells. He believes the new approach of what he terms “analog synthetic biology” will create a new set of fundamental and applied circuits that can dramatically improve the fine control of gene expression, molecular sensing, computation and actuation.

The research was funded by MIT Lincoln Laboratory, the Office of Naval Research and the National Science Foundation.

Vallecaucano Raúl Cuero, distinguido como Científico Hispano 2013

ORIGINAL: El País (Cali)

Redacción de El País

Abril 13, 2013

Este hijo de Buenaventura será distinguido por el Museo de Ciencia e Industria de Tampa, Mosi.

El científico habla cuatro idiomas. Empezó sus estudios de Biología en la Univalle, obtuvo un Máster en la Universidad de Ohio y luego hizo un PhD en Microbiología en la Universidad de Strathclyde, Reino Unido.

Así es Raúl Cuero, el científico de Buenaventura que triunfa en la Nasa

El científico bonaverense Raúl Cuero tiene nacionalidad colombiana, inglesa y americana. Archivo El País

Los vallecaucanos tienen una nueva razón para sentirse orgullosos: el científico de Buenaventura, que trabaja en la Nasa, Raúl Cuero, fue escogido por el Museo de Ciencia e Industria de Tampa, Florida, (Mosi), como el Científico Hispano en el 2013.

El reconocimiento se llevará a cabo en una gala en el Mosi el 12 de octubre del presente año. Este es un premio que se ha entregado en los últimos once años para destacar “modelos y mentores para los jóvenes hispanos de la bahía de Tampa”. Entre los reconocidos están un cirujano, un ganador del Nobel de Química, un astronauta de la Nasa, un biólogo marino, el director del Instituto Smithsoniano y el del Museo Nacional de Historia Natural, entre otros.

Cuero, fundador y director científico del Parque de la Creatividad, donde trabaja con jóvenes inventores de Colombia y otros países, ha incursionado en la biotecnología y patentado varios inventos, tales como una molécula que protege la piel de los efectos de la radiación UV, para prevenir el cáncer de piel.

“Es un honor para el Mosi presentar este reconocimiento al doctor Raúl Cuero. Como presidente del International Park Of Creativity creo que hay un vínculo directo de él con nuestra misión y principal ideología, que es hacer ciencia y demostrar el poder de la educación a los jóvenes”, dijo Wit Ostrenko, presidente del Mosi.

Entre tanto, el Director del Programa Presidencial Afrocolombiano, Óscar Gamboa Zúñiga, en nombre del Gobierno Nacional, felicitó al científico vallecaucano.

“El Programa Presidencial Afrocolombiano expresa su más sincera felicitación al doctor Raúl Cuero, quien es un orgullo y ejemplo de superación y progreso del pueblo afrocolombiano. Invito a las nuevas generaciones a emular a este gran científico, para orgullo de ellos mismos, del país, sus familias y la sociedad en general”, aseguró.

Cuero actualmente tiene 19 invenciones, la mayoría de ellas patentadas, y tiene 110 publicaciones científicas en los campos de biología, microbiología, biología molecular y biología sintética.

También es el autor de dos libros. Escribió ‘De Buenaventura a la Nasa. Entre el triunfo y la supervivencia’, impreso en inglés y español, que es su autobiografía desde su modesta crianza en Buenaventura, hasta llegar a Estados Unidos. En el 2012 publicó su nuevo libro, titulado ‘Cómo ser creativo para triunfar, la mente de la mente’, que ha sido traducido a cuatro idiomas.

Bedeviled by Dengue

ORIGINAL: The Scientist

By Beth Marie Mole

March 1, 2013

The global spread of dengue virus has immunologists and public-health experts debating the best way to curb infection.

DAVID SCHARF/GETTY IMAGES©

In 1961, during the first dengue outbreak physician Scott Halstead ever witnessed, children poured into Bangkok’s hospitals, passing and vomiting blood, faint from blisteringly high fevers. Twenty percent of the children would die within a few days as doctors scrambled to find treatments, with some in nearby Vietnam even plunging children into ice baths in an attempt to hold down their soaring temperatures.

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The deadly illness caused by dengue virus wasn’t yet known as dengue in Thailand; doctors there referred to it as “Chinese medicine poisoning” based on a demographic quirk. Although half the city’s population was Chinese, the only time Thai doctors—who practiced Western medicine—treated Chinese children was when the children had been stricken with this mysterious, deadly illness. Thus, doctors imagined that a horrific poisoning caused by Eastern remedies was responsible for the influx of Chinese patients. Instead, Halstead explains, Chinese parents had quickly learned that the hospital, rather than traditional medicine, was the best bet—however slim the chances—for defeating dengue.

Halstead who was drafted into the US Army after World War II and originally sent to Japan in 1957 to study encephalitis, had just settled into a lab across the street from the Children’s Hospital in Bangkok. “Everything I’ve ever done,” he says in retrospect, “is related to the treatment of dengue.” In the years that followed, he and his colleagues identified dengue as the cause of the outbreak and began tracking the four different versions of the virus, each transmitted by mosquitoes. Among their seminal discoveries, the researchers learned that the hemorrhagic disease that they saw in 1961 was most common when a child is infected with a second type of dengue—a finding that would prove pivotal in the decades-long search for a vaccine that continues today.

The World Health Organization estimates that more than 2.5–3 billion people, or more than 40 percent of the world’s population, are now at risk of being infected with dengue—including some in the developed world.http://www.the-scientist.com/images/March2013/dengue_virus.jpg

But as research efforts have evolved, so has the reach of dengue infections. The disease has now become prevalent in more than 100 countries, causing as many as 100 million infections per year. And it’s still spreading. The World Health Organization (WHO) estimates that more than 2.5–3 billion people, or more than 40 percent of the world’s population, are now at risk of being infected with dengue—including some in the developed world. In the past few years, cases of dengue have popped up in Texas, Florida, France, and Croatia. Of the 500,000 cases of severe dengue requiring hospitalization and the roughly 24,000 deaths they cause each year, most are in children, according to the WHO. And control measures have been met with challenges. One high-profile vaccine trial conducted by the French vaccine company Sanofi Pasteur partially failed last year, leaving investigators scratching their heads. The defeat comes amid fears of some researchers that vaccines have the potential to exacerbate a dengue infection rather than protect against it. “We’re in a mess,” Halstead says bluntly.

Going viral

When Halstead started digging into deng width="820" width="820"ue in the 1960s, only a handful of countries were home to all four types of the virus, which represent four separate viral jumps from monkeys to humans between 100 to 800 years ago, according to the US Centers for Disease Control and Prevention (CDC). But in the decades since, the four types—simply called dengue 1, 2, 3, and 4—have independently made their way around the globe. Poor urban planning and warming climates are partly to blame, having opened new territories to the mosquitoes that carry the virus, and global travel and trade have provided the necessary transit.

Tires may be the best example of mosquito and dengue transport: shipped across the globe on barges, tires collect water rings that offer mosquitoes first-class tickets to new locations. Consequently, dengue’s vectors, Aedes aegypti (the yellow fever mosquito) and A. albopictus (the tiger mosquito), have surged in new locations in Central and South America, Australia, and even in the lower United States. The yellow fever mosquito is particularly insidious, biting during the day, and able to spawn in water-filled crannies no larger than a small cup. Its eggs can withstand drought conditions, allowing the populat width="820" width="820" width="820" width="820"ion to quickly bounce back after a dry spell. It is now a common pest of dense urban areas—bringing disease with it.

After a cluster of dengue infections struck continental Europe, the European Union (EU) provided funding in 2011 for researchers to assess where dengue would strike next, amid fear that dengue would continue to spread in the developed world. The disease has traveled so quickly that “we only have estimates of the global burden of dengue, which is astonishing,” says epidemiologist Simon Hay of Oxford University, who is part of a consortium that’s developing risk maps of future dengue spread. The group is currently working on a map of where the disease exists now; only later will it work on how warming climates and city sprawl might change the map, says Jane Messina, the head medical geographer on the project.

Concerns have flared over the possibility that dengue could easily become endemic in Europe and in the United States, which had its own cluster of infections in 2012 in Texas and Florida. Ae. aegypti is now found in 23 states and A. albopictus in 26. “Dengue can occur anywhere the mosquito vectors occur,” says Ronald Rosenberg, the associate director of the CDC’s division of vector-borne diseases and a member of the WHO’s committee on neglected tropical diseases.

Concerns have flared over the possibil width="820" width="820"ity that dengue could easily become endemic in Europe and in the United States.

If experience from abroad is any indication, the economic impact of a dengue epidemic could be huge. Though severe disease is usually rare, it creates a big burden on health-care systems, says microbiologist and dengue expert Aravinda de Silva, of the University of North Carolina at Chapel Hill, who works in Sri Lanka where dengue has long been endemic. “Hemorrhagic fever is a massive concern. Every parent is terrified of their child getting it,” he explains. Parents often bring their children into the hospital at the first sign of dengue infection, which leads to many unnecessary hospitalizations—and the costs add up. With precautionary care as well as treatments for those who do get severe disease, dengue outbreaks weigh heavily on local economies—an outbreak in Thailand in 1994, for instance, cost an estimated $51 million, not including dengue prevention programs. Such an economic strain has brought the infection to the top of priority lists in health ministries around the world.

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The global spread of dengue over the past 3 decades, however, has driven more resources to research on how the virus spreads and how it can be defeated.

Catching a virus

Before the name “dengue” caught on in the Americas, it was often referred to as “breakbone fever,” or la quebradora in Spanish. The nickname refers to the crippling aches that come with infection. Once delivered by a mosquito, dengue virus hijacks skin and some immune cells and hitchhikes through the lymphatic system, infecting other tissues and organs and loading the bloodstream with viral replicates. The body’s immune system counters with blazing inflammation, causing sharp pains in muscles. Eighteenth-century reports of dengue infection describe the wretched gaits of patients as they staggered on swollen limbs, often in a stupor from fever.

For the lucky, those will be the worst of their symptoms. Others, however, can develop life-threatening disease. If the inflammation firestorm gets out of hand, it can damage the lining of capillaries—the smallest blood vessels—causing gaps through which blood plasma can seep. Systemic internal leaking quickly leads to a drop in blood pressure, followed by shock, organ failure, and massive bleeding.

Between 2005 and 2007, Managua, Nicaragua, saw a mysterious spike in the number of children entering hospitals with dengue hemorrhagic fever and shock syndrome. Since the 1980s, the neighborhoods around the city had been riddled with Ae. aegypti as well as the four dengue types they carry, but no one knew why so many more children were suddenly developing severe disease. Infectious disease researcher Eva Harris and her team from the University of California, Berkeley, and the Nicaraguan Ministry of Health had been working on infectious disease there for decades, and noticed severe dengue disea width="820"se occurred in children reinfected with a second type of the virus, similar to the pattern Halstead saw in the 1960s with second infections.

Simona Zompi, an immunologist working on Harris’s team, was dissecting the immune system’s response to dengue. When a person is initially infected, the dengue viral particles attack skin and immune cells by latching onto receptors on the cell surface. The cells enclose the viruses in a sac—a process called receptor-mediated endocytosis—that would normally digest the viral captives with enzymes in an acidic milieu, like a piece of food in the stomach. But dengue virus particles escape digestion by rearranging their envelope proteins to fuse with the sac’s membrane, opening a channel through which the capsid-encoated viral genome is released into the infected cell’s cytoplasm. Once free, the virus usurps the cell’s machinery to create a viral factory, triggering a full-blown dengue infection.

Zompi and the team focused on B cells, which react to the infection by creating antibodies against the infecting virus. Once the virus is defeated, some of these cells go into hibernation as memory B cells, which become quickly reactivated upon reinfection with dengue for the rest of the person’s life. Those antibodies normally foil infection by blanketing the viral particle, which prevents the virus from binding to cell receptors and entering cells. The antibody-coated virus is then taken up by monocytes or macrophages, which, after endcytosis, can digest the invader because the coated particle is unable to escape the digestive sac. (See illustration below.)

FREQUENT CHECKS: A young girl is examined by a military doctor 45 miles away from Rio de Janeiro, Brazil. The Brazilian military set up three field hospitals to help manage patients with dengue infections.© ANTONIO SCORZA/AFP/GETTY IMAGES

However, this protective immune response depends on whether antibodies can bind strongly enough to coat and disable—or neutralize—the virus, Zompi explains. Some antibodies bind poorly to the viral particle and, as a result, only a few manage to cling to the virus, which is just enough to entice macrophages and monocytes to engulf them. However, without complete antibody coverage of the viral coat, the virus can still escape from the endocytic sacs of the macrophages or monocytes and take over the very cells that have engulfed it. (See illustration below.) Now, the virus has an additional pathway to enter cells: all of the immune cells recruited and activated by the antibodies could potentially become virus-producing factories. Thus, antibodies with poor binding affinity and neutralizing potential effectively boost the infection, and the inflammatory response can crank to inferno levels, causing hemorrhagic fever and shock syndromes. Scientists refer to this explanation for severe disease as “antibody-dependent enhancement” (ADE) of the immune response.

Most antibodies generated against a specific dengue type, dengue 1 for example, will bind well and be able to thwart future infections of that type. But when a new type of dengue invades—dengue 2, for instance—the reactivated dengue 1 antibodies may only partially recognize the virus and thus lead to ADE. Indeed, Harris and Zompi found that as the predominant circulating dengue virus type switched in Managua, patients hospitalized with dengue made the strongest antibody response to a dengue type from a previous infection, not the current infecting dengue type. And most countries are infested with the four types of dengue that can fluctuate in prevalence.

Some researchers worry that vaccines designed to spur antibody production might instead trigger ADE if the B cells generate low-affinity antibodies rather than those that completely blanket the virus. If that were the case, being vaccinated could predispose children to ADE.

Vaccine development dissension

ANTIBODY-DEPENDENT ENHANCED (ADE) IMMUNITY ©TAMI TOLPA

But not all dengue researchers are convinced that severe disease can be explained by the ADE response, says de Silva. There are two competing hypotheses about how severe hemorrhagic and shock diseases might unfurl: other immune cells, such as T cells, may present different fragments of the virus to the immune system, stimulating a greater inflammatory response; or, more virulent subtypes of each of the dengue types may trigger the more severe immune reaction characteristic of ADE. But the antibody hypothesis is certainly the front-runner, de Silva says—especially after his recent discovery of how dengue-neutralizing antibodies work.

During initial infection, the human immune system makes a range of antibodies with different affinities to the virus. The antibodies capable of neutralizing the virus apparently latch onto a wedge between two adjacent molecules of an envelope protein on the coat of the intact virion. The new finding is significant because it casts doubt on past immunology and vaccine-development studies that have focused on generating an antibody response against only a small fragment of the envelope protein in isolation. Antibodies that don’t neutralize the virus by binding to the wedge may be candidate ADE generators, says de Silva.

Yet many researchers in the field are reluctant to acknowledge the new complication, says Halstead. “A lot of people don’t like to have to address [the possibility of ADE] head on,” he says.

Indeed, current recommendations by the WHO on conducting clinical trials of candidate dengue vaccines don’t include specific guidelines for ADE. In fact, ADE and its potential causes are considered a hypothetical concern that should not interfere with development of a vaccine, according to the WHO.

“[ADE] may not be a concern, in my own opinion,” says infectious-disease researcher Claire Huang, of the CDC’s division of vector-borne diseases, echoing the WHO’s stance. Along with a team of researchers at the CDC, Huang has been toiling for years to develop an effective vaccine, and is working with the commercial vaccine developer Inviragen on a vaccine now in Phase 2 clinical trials. It may be more complicated, she adds, but most antibody responses are protective and robust.

The vaccine she’s been working on is tetravalent, meaning it’s designed to generate antibodies against all four types of dengue. Huang and her team borrowed the genetic backbone of an earlier successful vaccine against the type 2 virus, and dressed that genome, with its attenuating mutations, in the other three viral coats, creating four recombinant viruses. “From the outside, they all look like either dengue 1, dengue 2, dengue 3, or dengue 4, but inside they’re all the same attenuated virus,” she explains. The team hopes that the vaccine will produce a suite of neutralizing antibodies against all types of dengue.

So far, the results look promising. The vaccine sailed through Phase 1 trials, proving safe in healthy children and adults in Colombia and the U.S. who had no prior exposure to dengue. But the earlier tetravalent vaccine made by Sanofi Pasteur also had great early results. After buzzing through initial safety tests and Phase 2 trials, that vaccine moved to a Phase 2b trial, which enlisted 4,000 school-age children in Thailand’s Ratchaburi Province. The vaccine required three shots over the course of a year, and in September the company revealed that only 30 percent might be protected, although none of the results were statistically significant.

“I looked at the vaccine results and wondered if they had given people water,” Halstead says. “It was very surprising,” echoes de Silva. It’s still unclear what went wrong, he says. The vaccine showed 80 to 90 percent protection against dengue types 3 and 4, and around 60 percent protection against dengue 1. But it failed at protecting against dengue 2—the dengue that was circulating that year at high levels. The question we’re left with, de Silva says, is whether that virus was just a mismatch with the vaccine, or if the dengue 2 portion of the vaccine simply didn’t generate a good antibody response in the vaccinated children.

The only triumph of the trial was that it didn’t show an increase in severe disease. Of the 4,000 children vaccinated, only five developed severe disease. “The vaccine was still very safe,” says Dan Stinchcomb, cofounder and CEO of Inviragen. “[The Sanofi] vaccine is somewhat similar to ours, and the trial laid to rest one of the biggest concerns,” he says. The study demonstrated “that if you’re not fully protected against all four viruses, then you’re not more susceptible to severe disease,” or ADE.

But Halstead points out that the trial only followed children for a year—not long enough for them to become infected a second time. In that time frame, it’s impossible to know if the risks of ADE are actually diminished, he says.

A different angle

In the meantime, others are looking to non-vaccine strategies to contain the disease. Despite the potential for spread in the developed world, most global health experts are focused on developing countries. With advanced water-management systems, responsive public-health programs, and effective disease monitoring, dengue outbreaks in the U.S. or Europe have a good chance of being quashed quickly, says Rosenberg. “The risk pales in comparison to the daily risk of getting dengue in the tropics,” he adds.

Because of logistical barriers in developing countries, some experts doubt that vaccines are the best answer to the dengue problem. “Implementing a vaccine is difficult,” says Rosenberg. For example, 

Tags virology, vaccine design, vaccine, public health, microbiology, infectious disease, immunology, dengue virus and dengue infectionif the vaccine requires multiple boosters, most people in low-income communities will have difficulty receiving and/or affording all of the doses. “It’s unlikely that the vaccine is going to be the panacea for controlling dengue,” he says.

KIDS AT RISK: Young victims of dengue fever crowd the children’s ward of the government-run Quirino Memorial Hospital in Manila on September 11, 2010. © AFP/GETTY IMAGES

In the absence of an effective vaccine or a halt to mosquito breeding, clinicians have honed the art of treating severe disease. With no infection-specific protocol, doctors treat severe disease by compensating for lost fluids, which is akin to constantly pumping up a punctured tire. The challenge is to maintain a patient’s blood pressure at a high enough level to circulate blood without going too far and “popping” the system, thus causing life-threatening edemas that saturate the lungs or brain. This is tricky to do in adults, but even trickier in infants and children, who are more likely to develop the disease.

However, more and more doctors are beginning to learn best practices for controlling the disease. In Bangkok, where Thai clinicians are at the forefront of clinical case management, a 20 percent mortality rate of dengue-infected patients in the 1960s is now down to just 0.1 percent. Doctors and nurses convene after each death to discuss in painstaking detail what went wrong. Clinicians now have such a fine understanding of the physiology of the disease—and how to track and control it by monitoring vital signs and urine output, and administering delicate fluid therapies while monitoring plasma volume—that death is avoidable, says de Silva.

In Nicaragua, Harris and UC Berkeley-based researcher Josefina Coloma are working with an international nonprofit group to spur grass-roots community projects to educate residents about the mosquito life cycle, and to motivate them to eliminate standing water that can be a breeding ground for Ae. aegypti. Their preliminary findings showed that community efforts were able to reduce dengue infection. Simply informing people of the link between standing water and disease transmission has had an important impact, Harris says.

Indeed, the inability to keep dengue from spreading is a shame, Halstead says. Despite advanced research, he argues, dengue is a disease of medieval sanitation and water systems, irresponsible urbanization, and a lack of basic education about disease spread. “If we stop dengue by immunizing,” without mosquito controls and other prevention methods, Halstead says, “then I would say that human beings have copped out. If dengue [only] ends because of a dengue vaccine, then we’ve failed in our public-health efforts.”

Could the sea be conscious? Research reveals how tiny plankton behave like a marine 'megamind'

ORIGINAL: Daily Mail

By DAMIEN GAYLE

13 February 2013

U.S. researchers find that different forms of picoplankton react as one to environmental changes

Although as different as humans and fungi, the creatures' behaviour was linked

Findings could help researchers understand why some species are impossible to grow in isolation

Vastly different species of sea microbes work together to respond as one to their surroundings as if they have one 'megamind', new research has revealed.

U.S. researchers have discovered communities of infinitesimal creatures in our oceans react in unison to changes in their environment.

The links between them are not well understood, but findings suggest the creatures rely on each other to almost the same extent as the different cells in a human body.

Megamind: Despite the amazing diversity of marine microbes, a new research paper shows that many different groups work together to react in unison to their surroundings

As an example, if one set of the microbes were, say, creating energy through photosynthesis, which would then produce carbon dioxide, another set of microbes would somehow know and react - perhaps preparing to absorb the carbon dioxide.

The open sea contains an amazing diversity of extremely tiny organisms called picoplankton, which include relatively simple life forms such as marine bacteria, as well as more complicated organisms.

Microbiologists who study wild marine microbes, as opposed to the lab-grown variety, face enormous challenges in getting a clear picture of the daily activities of their subjects.

To take a look at these creatures in their natural habitat, researchers from the Massachusetts Institute of Technology and the Monterey Bay Aquarium Research Institute used a new method for collecting marine microbes.

They created a robotic sampling device which dangled beneath the waves to collect samples of one billion microbes every four hours.

Similar to fast photography that stops action, the robotic device 'fixed' each sample so that whatever genes the microbes were expressing at the moment of capture were preserved for later study.

After returning the samples to the lab, researchers used cutting-edge analysis techniques to figure out which genes within the microbes were actively being used at different times of day.

This involved sorting through millions of billions of fragments of genetic material and then assigning each fragment to a specific gene and a specific type of microbe.

In so doing they created a time-lapse montage of the daily labours of a range of microbial species over a two-day period.

A research vessel drifts near the buoy supporting the Environmental Sample Processor used to collect microbes for the experiment. Inset shows the yellow float with the ESP pressure housing suspended in the water

'A naturalist like Sir David Attenborough can follow a herd of elk and see how the elk’s behavior changes hour to hour, day to day and week to week,' said Edward DeLong, professor of environmental systems at MIT.

HOW RESEARCHERS 'FROZE TIME' TO MAKE THEIR FINDINGS

Using their robot microbe collecting device, researchers were able to gather samples of one billion microbes every four hours and keep them 'fixed' at the moment of collection.

This meant that whatever genes the microbes were expressing at the moment of capture were preserved for later study in the lab.

Microbes are extraordinarily sensitive to slight environmental changes, altering their gene expression rapidly in response to fluctuations in temperature, light, nutrient availability and other environmental variables.

Because of this, the genes they express tell a story about their habitat and their interactions with it.

In essence, changes in their gene expression provide information on the good times and the bad times they experience.

In a sense, each naturally occurring microbe is a living sensor and the researchers can read the sensors’ outputs by studying their gene expression.

By studying these environmental responses the MIT/MBARI team were able to make completely new findings about the behaviour of the creatures.

'But we haven’t been able to observe naturally occurring microbes with that kind of resolution until now.'

Professor DeLong, who is lead author of a paper in the Proceedings of the National Academy of Sciences detailing the research, added: 'We've essentially captured a day in the life of these microbes.

'As little as three years ago, I wouldn’t have even have considered it possible to get such a high resolution picture of microbial population dynamics and activity in the "real world".'

The montage showed photosynthetic microbes, which create the oxygen, energy and organic carbon used by the rest of the food web, ramped up their light-utilising activities in the morning and powered those down at night, just as their domestic brethren do in response to light and dark in the lab.

But the underwater scenes also showed something scientists had never seen before.

Non-photosynthetic, carbon-eating microbes of very different species displayed synchronised, rapidly varying metabolic gene expression - despite the fact that they came from groups as different as humans and fungi.

Some of the genes simultaneously expressed by different species shared the same function — for instance, genes associated with growth or respiration.

Others encoded very different functions, mirroring the varied metabolic capabilities of the disparate species.

'We've essentially captured a day in the life of these microbes': Researchers readying the robotic device connected to a buoy for its two-day sampling journey off the coast of California

The researchers hypothesised that all these microbes were reacting to the same environmental changes, but that different groups of microbes were responding in different ways.

Although the researchers cannot tell exactly which environmental changes the microbes were responding to, they suspect that the different groups of microbes were working together to obtain different types of food.

For example, some picoplankton could have been consuming large organic compounds such as proteins and fats. In the process, they could have produced simpler organic compounds, such as amino acids, which were then released into the surrounding seawater and consumed by other picoplankton.

'These results show a surprising amount of coordination between marine microbes,' said a spokesman for the Monterey Bay Aquarium Research Institute.

'They also suggest that, as in the food webs of larger organisms, many different groups of marine microbes rely on each other to survive on a day-to-day basis.

'This could help explain why so many species of marine microbes are difficult or impossible to grow by themselves in the lab.'