Scientists Shocked To Discover Eukaryote With NO Mitochondria

photo credit: The microbe was actually found living in the gut of a chinchilla. Dr. Naoji Yubuki

For a long time it has been thought that all eukaryotes – organisms in which the DNA is enclosed in a membrane including almost all life we can see – had to contain mitochondria. Known as the “power house” of the cell, these little subunits within the cell provide the organisms with energy and were thus thought to be essential. But it now seems that actually they might not be that essential, as researchers describe the first eukaryote known that lacks mitochondria.

Other eukaryotes had been previous contenders for the title, such as the microbe Giardia intestinalis from the gut, but further investigations had found that they simply contained highly reduced mitochondria difficult to observe. But after checking another candidate from the genus Monocercomonoides, isolated from a sample retrieved from the gut of a chinchilla owned by one of the lab members, the researchers of this latest study found no trace of the organelles at all after a genetic analysis looking for mitochondrial genes.

“In low-oxygen environments, eukaryotes often possess a reduced form of the mitochondrion, but it was believed that some of the mitochondrial functions are so essential that these organelles are indispensable for their life,” explains Anna Karnkowska, co-author of the study describing the new finding published in Current Biology. “We have characterized a eukaryotic microbe which indeed possesses no mitochondrion at all.”

Because the gut is such a low oxygen environment, many microbes that call it home already have reduced mitochondria. Coupled with the fact that they are living in an environment surrounded by nutrients, the researchers think that the Monocercomonoides merely has no need for the organelles, and so have lost them. They think instead that the microbes simply absorb the nutrients directly from their surroundings, and then break them down with enzymes in order to get energy.

Yet they also face another problem, because mitochondria do another task as well as provide the cell with energy: They also give the cell vital clusters of iron and sulfur that are needed by various proteins. To solve this, it seems like the Monocercomonoides microbe has “borrowed” genes from bacteria to give them a “cytosolic sulfur mobilization system,” which fulfils the mechanism usually found in the mitochondria.

While all the evidence seems to stack up, others suggest that the researchers will need to double check. Either way, it’s looking more and more likely that textbooks may have to be rewritten, as the researchers suspect that there are probably other microbes that also lack the organelles. “This amazing organism is a striking example of a cell which refuses to adhere to the standard cell biology textbook, and we believe there may be many more similar examples in the so far hidden diversity in the world of microbial eukaryotes, the protists,”says Karnkowska. 

ORIGINAL: IFLS

by Josh L Davis

May 13, 2016

Mitochondria trigger cell aging, study shows

Dr. Clara Correia-Melo and Dr. Joao Passos are in the lab. Credit: Newcastle University

An international team of scientists has for the first time shown that mitochondria, the batteries of the cells, are essential for ageing.

In a study, published today in the EMBO Journal and led by Dr João Passos at Newcastle University, they found that when mitochondria were eliminated from ageing cells they became much more similar to younger cells. This experiment was able for the first time to conclusively prove that mitochondria are major triggers of cell ageing.

This brings scientists a step closer to developing therapies to counteract the ageing of cells, by targeting mitochondria.

Defying ageing in the cell

As we grow old, cells in our bodies accumulate different types of damage and have increased inflammation, factors which are thought to contribute to the ageing process.

The team carried out a series of genetic experiments involving human cells grown in the laboratory and succeeded in eliminating the majority, if not all, the mitochondria from ageing cells. Cells can normally eliminate mitochondria which are faulty by a process called mitophagy. The scientists were able to "trick" the cells into inducing this process in a grand scale, until all the mitochondria within the cells were physically removed.

Dr. Joao Passos and Dr. Clara Correia-Melo in the lab. Credit: Newcastle University

To their surprise, they observed that the ageing cells, after losing their mitochondria, showed characteristics similar to younger cells, that is they became rejuvenated. The levels of inflammatory molecules, oxygen free radicals and expression of genes which are among the makers of cellular ageing dropped to the level that would be expected in younger cells.

New thinking on mitochondria

Dr João Passos of the Institute for Ageing said: "This is a very exciting and surprising discovery. We already had some clues that mitochondria played a role in the ageing of cells, but scientists around the world have struggled to understand exactly how and to what extent these were involved.

"These new findings highlight that mitochondria are actually essential to the ageing of cells."

The team led by Newcastle University and involving other universities in the UK and the US, also deciphered a new mechanism by which mitochondria contribute to ageing. They identified that as cells grow old, mitochondrial biogenesis, the complex process by which mitochondria replicate themselves, is a major driver of cellular ageing.

"This is the first time that a study demonstrates that mitochondria are necessary for cellular ageing," said Dr Clara Correia-Melo of the Newcastle University Institute for Ageing and the lead author of the study. "Now we are a step closer to devising therapies which target mitochondria to counteract the ageing of cells."

Explore further: Stem cells overcome damage in other cells by exporting mitochondria

More information: Mitochondria are required for pro-ageing features of the senescent phenotype. EMBO Journal. DOI: 10.15252/embj.201592862

Journal reference: EMBO Journal

Provided by: Newcastle University

ORIGINAL: MedicalXpress

February 4, 2016

New mitochondrial DNA editing technique prevents genetic diseases in mice

Image: Wire_man/Shutterstock

And it could prevent the transmission of incurable diseases from mother to child.

A new technique to edit mitochondrial DNA has been tested on mice, and if replicable in humans, could help prevent mothers living with certain incurable disease from passing them onto their children, researchers say.

Mitochondria are tiny powerhouses found inside nearly all human cells, and are responsible for generating the chemical energy that allows our cells to perform many essential functions. For example, this energy enables communication between brain cells, and it allows our muscle cells to keep us moving around.

However, defects in these cellular components, which have their own DNA, can lead to a range of incurable conditions, known collectively as mitochondrial diseases. 

While the diseases present differently in each individual, they can generally be characterised by symptoms such as poor muscle development and weakness; hearing, vision and other neurological impairments; learning disabilities; and heart, liver, gastrointestinal and respiratory diseases.

For thousands of women around the world living with one of these incurable diseases, having children is a gamble, as it's likely their defective mitochondrial DNA will be passed on.

Now, researchers at the Salk Institute for Biological Studies in the US have developed a technique to eliminate mitochondrial mutations from eggs or early embryos, while leaving the healthy mitochondria intact.

The proof-of-concept demonstration, which has been described in the journal Cell, could help prevent children from inheriting these chronic diseases.

The researchers used to two different enzymes - or nucleases - inside cells, which can be engineered to cut specific strands of nucleic acid, functioning kind of like 'molecular scissors'. 

As Smitha Mundasad from the BBC reports, the team tested the "molecular scissors on mice with two different types of mitochondrial DNA (mtDNA). They were able to recognise and cut out disease-causing mtDNA in mouse embryos."

The mice offspring were born healthy and developed naturally into adulthood without any diseases, the researchers say.

"We might not be able to eliminate 100 percent of the mutated copies of mitochondrial DNA," said lead author Pradeep Reddy in a press release. "But you don't need to eliminate all of the mutated copies: just reducing the percentage significantly enough can prevent the disease in the next generation."

The team also successfully demonstrated their technique on defective human mitochondrial DNA, which had been inserted into mouse eggs.

Stem cell scientist Duscko Ilic from King's College London in the UK, who was not involved in the research, told the BBC that the group's method for correcting mitochondrial defects was a "technical masterpiece" but said it was unlikely to make it to clinical trials in near future.

"Replacing faulty genes in human pre-implantation embryos, germ cells or gametes poses serious risks," Ilic said.

Another independent expert, geneticist Frances Flinter from Guy's and St Thomas' Hospital in the UK, told the BBC: "The biggest question to address will be the possibility that DNA cutting enzymes may disrupt adjacent genes that are important, leading to unintended adverse consequences." 

While the results seen in mice are promising, there's obviously a long way to go before this technology can be used to help humans. And the route to clinical trials might become increasingly murky given the concerns over gene editing, which have resurfaced in a big way after Chinese scientists admitted to tweaking the genes of human embryos. 

Source: BBC

Via: Science Alert

By MYLES GOUGH

27 APR 2015