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Why does mitochondria DNA only come from mom?

Like most cells, sperm contain energy-producing mitochondria. However, once a sperm fertilizes an egg its own mitochondria break down. Scientists have a new clue to why the most mitochondrial DNA is passed down to children from their mothers — and not their fathers.


Sperm DNA inside mitochondria (energy-producing organelles) is typically destroyed as fertilization of an egg begins. A protein called CPS-6 cuts apart male mitochondrial DNA to stop any proteins that might be produced. Researchers believe this is done to prevent sperm mitochondria from hurting a developing embryo.The research results are reported in the magazine Science.


“This is a very long-standing mystery in biology — why — in so many organisms — [only] maternal mitochondria are inherited.”

Ding Xue PhD, Geneticist, University of Colorado Boulder, USA and team leader.


It is estimated that around 1.5 billion years ago of years ago, mitochondria were independent, free-living bacteria which became incorporated into endosymbiont relationships (when an organism lives within the cells of another organism). Today, mitochondria live within the human organ system producing energy for us. They are referred to as "the powerhouse of the cell" because they generate most of the cell's supply of adenosine triphosphate (ATP), used as a source of chemical energy. A human egg contains about 200,000 mitochondrial DNA (mtDNA) molecules — while a healthy human sperm averages about 5 molecules. In 1999 it was found sperm mitochondria are marked with ubiquitin (a compound which plays a role in degrading defective and/or superfluous proteins) to target them for destruction.

Mitochondria always have their own genomes, although their DNA is simpler and shorter than DNA found in the nucleus of a cell. But their genomes also have far fewer genes than nuclear DNA. Xue and his collaborators used electron microscopes to watch as sperm from the worm Caenorhabditis elegans (c elegans) fertilized eggs. They watched as paternal mitochondria broke down from the inside out. To identify which gene might be responsible for this process, researchers then looked at what changed when certain genes weren’t working. That process identified a gene producing the protein CPS-6.

CPS-6 normally controls programmed cell death to help organisms keep old and new cells in balance. But Xue’s team found that during fertilization, CPS-6 also moves into the innermost part of the mitochondria and chops paternal DNA into pieces. And CPS-6 doesn’t work alone. Other scientists had previously identified that the process of autophagy (Greek auto- "self" and phagein "to eat") assists in the break down of paternal mitochondria (Science News: 1/1/2000).  Autophagy recruits structures in the egg to carry away pieces of paternal mitochondria like a team of garbage collectors. The two processes work together. Without CPS-6 acting as a flag, autophagy machinery didn’t cart away the unwanted mitochondria as quickly.


“Our study for the first time shows that paternal mitochondria actually cooperate with maternal degradation machinery to ensure that sperm mitochondria are all removed.”

Ding Xue PhD, Department of Molecular, Cellular, and Developmental Biology, University of Colorado, Boulder, CO, USA.


Interestingly, if mitochondria removal became delayed, embryo death increased. This observation suggests that paternal mitochondria are identified as interfering with normal development, but scientists are still not sure exactly how.

It’s also not yet clear how directly the mechanism seen in c elegans carries over to humans. “You could imagine there’s a similar mechanism, but there’s no demonstration yet,” explains Vincent Galy, a biologist at the Pierre and Marie Curie University in Paris who was not involved in the work.

Although the CPS-6 protein is similar to one found in humans, and it controls cell death similarly in both flies and mice species, exactly when sperm lose their mitochondria also varies from species to species, so the process itself probably varies slightly in humans too.

Abstract
Oligonucleosomal fragmentation of chromosomes in dying cells is a hallmark of apoptosis. Little is known about how it is executed or what cellular components are involved. We show that crn-1, a Caenorhabditis elegans homologue of human flap endonuclease-1 (FEN-1) that is normally involved in DNA replication and repair, is also important for apoptosis. Reduction of crn-1 activity by RNA interference resulted in cell death phenotypes similar to those displayed by a mutant lacking the mitochondrial endonuclease CPS-6/endonuclease G. CRN-1 localizes to nuclei and can associate and cooperate with CPS-6 to promote stepwise DNA fragmentation, utilizing the endonuclease activity of CPS-6 and both the 5′–3′ exonuclease activity and a previously uncharacterized gap-dependent endonuclease activity of CRN-1. Our results suggest that CRN-1/FEN-1 may play a critical role in switching the state of cells from DNA replication/repair to DNA degradation during apoptosis.

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Jul 4, 2016   Fetal Timeline   Maternal Timeline   News   News Archive   


Mitochondrial DNA are the small circular chromosomes found inside mitochondria.
These organelles are found at the sites of energy production and are passed from mother to child.

Image Credit: National Institutes of Health. National Human Genome Research Institute.
'Talking Glossary of Genetic Terms. April 25, 2012 — http://www.genome.gov/glossary/


 


 

Phospholid by Wikipedia