Posts about mitochondria

Unexpected Risks Found In Editing Genes To Prevent Inherited Disorders

Mitochondrial replacement seeks to remove genes known to cause genetic defects from embryos in order to allow for a baby to avoid inheriting the defect.

Mitochondrial Replacement Techniques: Ethical, Social, and Policy Considerations from the USA National Academy of Sciences

Accordingly, the committee recommends that any initial MRT clinical investigations focus on minimizing the future child’s exposure to risk while ascertaining the safety and efficacy of the techniques. The recommended restrictions and conditions for initial clinical investigations include

  • limiting clinical investigations to women who are otherwise at risk of transmitting a serious mtDNA disease, where the mutation’s pathogenicity is undisputed, and the clinical presentation of the disease is predicted to be severe, as characterized by early mortality or substantial impairment of basic function; and
  • transferring only male embryos for gestation to avoid introducing heritable genetic modification during initial clinical investigations.

Following successful initial investigations of MRT in males, the committee recommends that FDA could consider extending MRT research to include the transfer of female embryos if clear evidence of safety and efficacy from male cohorts, using identical MRT procedures, were available, regardless of how long it took to collect this evidence; preclinical research in animals had shown evidence of intergenerational safety and efficacy; and FDA’s decisions were consistent with the outcomes of public and scientific deliberations to establish a shared framework concerning the acceptability of and moral limits on heritable genetic modification.

The research in this area is interesting and our ability to help achieve healthy lives continues to grow. The path to a bright future though is not without risk. It requires careful action to pursue breakthrough improvements while minimizing the risks we take to achieve better lives for us all.

Unexpected Risks Found In Editing Genes To Prevent Inherited Disorders

Earlier this month, a study published in Nature by Shoukhrat Mitalipov, head of the Center for Embryonic Cell and Gene Therapy at the Oregon Health and Science University in Portland, suggested that in roughly 15 percent of cases, the mitochondrial replacement could fail and allow fatal defects to return, or even increase a child’s vulnerability to new ailments.

The findings confirmed the suspicions of many researchers, and the conclusions drawn by Mitalipov and his team were unequivocal: The potential for conflicts between transplanted and original mitochondrial genomes is real, and more sophisticated matching of donor and recipient eggs — pairing mothers whose mitochondria share genetic similarities, for example — is needed to avoid potential tragedies.

“This study shows the potential as well as the risks of gene therapy in the germline,” Mitalipov says. This is especially true of mitochondria, because its genomes are so different than the genomes in the nucleus of cells. Slight variations between mitochondrial genomes, he adds, “turn out to matter a great deal.”

Related: Gene Duplication and EvolutionThe Challenge of Protecting Us from Evolving Bacterial ThreatsOne Species’ Genome Discovered Inside Another’s (2007)Looking Inside Living Cells

An Eukaryote that Completely Lacks Mitochondria

If you don’t have any idea what the title means that is ok. I probably wouldn’t have until the last 15 years when I found how interesting biology is thanks to the internet and wonderful resources online making biology interesting. I hope you find learning about biology as interesting as I do.

Look, Ma! No Mitochondria

Mitochondria have their own DNA, and scientists believe they were once free-living bacteria that got engulfed by primitive, ancient cells that were evolving to become the complex life forms we know and love today.

What they learned is that instead of relying on mitochondria to assemble iron-sulfur clusters, these cells use a different kind of machinery. And it looks like they acquired it from bacteria.

The researchers say this is the first example of any eukaryote that completely lacks mitochondria.

However, the results do not negate the idea that the acquisition of a mitochondrion was an important and perhaps defining event in the evolution of eukaryotic cells, he adds.

That’s because it seems clear that this organism’s ancestors had mitochondria that were then lost after the cells acquired their non-mitochondrial system for making iron-sulfur clusters.

Biology is amazing and mitochondria are one of the many amazing details. I wish so much that my education could have given biology a tiny fraction of the interest I have found it in after school.

Related: Human Gene Origins: 37% Bacterial, 35% Animal, 28% EukaryoticOne Species’ Genome Discovered Inside Another’sParasite Evolved from Cnidarians (Jellyfish etc.)Plants, Unikonts, Excavates and SARs

Funding Medical Research

Cheap, ‘safe’ drug kills most cancers

It sounds almost too good to be true: a cheap and simple drug that kills almost all cancers by switching off their “immortality”. The drug, dichloroacetate (DCA), has already been used for years to treat rare metabolic disorders and so is known to be relatively safe. It also has no patent, meaning it could be manufactured for a fraction of the cost of newly developed drugs.

Evangelos Michelakis of the University of Alberta in Edmonton, Canada, and his colleagues tested DCA on human cells cultured outside the body and found that it killed lung, breast and brain cancer cells, but not healthy cells. Tumours in rats deliberately infected with human cancer also shrank drastically when they were fed DCA-laced water for several weeks.

DCA attacks a unique feature of cancer cells: the fact that they make their energy throughout the main body of the cell, rather than in distinct organelles called mitochondria. This process, called glycolysis, is inefficient and uses up vast amounts of sugar.

Until now it had been assumed that cancer cells used glycolysis because their mitochondria were irreparably damaged. However, Michelakis’s experiments prove this is not the case, because DCA reawakened the mitochondria in cancer cells. The cells then withered and died

The University of Alberta is raising funds to further the research. Some look at this and indite a funding system that does not support research for human health unless there is profit to be made. Much of the blame seems to go to profit focused drug companies. I can see room for some criticism. But really I think the criticism is misplaced.

The organizations for which curing cancer is the partial aim (rather than making money) say government (partial aim or public health…), public universities (partial aim of science research or medical research…), foundations, cancer societies, private universities… should fund such efforts, if they have merit. Universities have huge research budgets. Unfortunately many see profit as their objective and research as the means to the objective (based on their actions not their claims). These entities with supposedly noble purposes are the entities I blame most, not profit focused companies (though yes, if they claim an aim of health care they I would blame them too).

Now I don’t know what category this particular research falls into. Extremely promising or a decent risk that might work just like hundreds or thousands of other possibilities. But lets look at several possibilities. Some others thoughts on where it falls: Dichloroacetate to enter clinical trials in cancer patients, from a previous post here – Not a Cancer Cure Yet, The dichloroacetate (DCA) cancer kerfuffle, CBC’s ‘The Current’ on dichloroacetate (DCA), Dichloroacetate (DCA) Phase II Trial To Begin (“Like hundreds (if not, thousands) of compounds being tested to treat cancer, DCA was shown by Michelakis’ group earlier this year to slow the growth of human lung tumors in a preclinical rodent model.”).
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Origins of the Domestic Cat

DNA traces origin of domestic cat:

The study suggests the progenitors of today’s cats split from their wild counterparts more than 100,000 years ago – much earlier than once thought. At least five female ancestors from the region gave rise to all the domestic cats alive today, scientists believe. DNA evidence suggests that, apart from accidental cross-breeding, European wildcats are not part of the domestic moggy’s family tree. Neither are the Central Asian wildcat, the Southern African wildcat, or the Chinese desert cat.

The earliest archaeological evidence of cat domestication dates back 9,500 years, when cats were thought to have lived alongside humans in settlement sites in Cyprus. However, the new results show the house cat lineage is far older. Ancestors of domestic cats are now thought to have broken away from their wild relatives and started living with humans as early as 130,000 years ago. The researchers focused on DNA in the mitochondria, the power plants of cells which supply energy and have their own genetic material.

Cool. Related: Cat HistoryDNA Offers New Insight Concerning Cat EvolutionMidichloria mitochondrii

Midichloria mitochondrii

Use the force, bacteria (sadly, the site broke the link so our link was removed):

When his team took a tick apart to look for the new bug, they found it in the ovaries. And, when they looked closely at electron micrographs of infected ovarian tissues, they could see that the microbes were intracellular – living not in the cytoplasm of tick ova, but within their mitochondria.

“We’d never seen anything like this before,” Lo says, as he opens the image files on his laptop on a rainy afternoon in Sydney. “They seem to get in between the inner and outer mitochondrial membranes and eat the mitochondria up. In the end you’ve just got this empty sack.”

says he wasn’t aware of any other bacteria that live inside mitochondria. “It’s pretty surprising to see a bacterial species living inside the mitochondrion, which itself was a bacterium,”

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