There is new evidence that the "mother's curse" - the possibility that moms may transmit genes to their children that harm their sons but not their daughters - holds true in animals.
Such a possibility arises because there are two independent parts of the genome in the eukaryote cells, which are found in plants and animals, and the two are locked in a "conflict-driven molecular arms race" that impacts human health and wellness. The lion's share of the genome is located in the cell nucleus. But there is also a much smaller secondary portion located in the mitochondria.
According to the generally accepted theory, mitochondria were originally independent bacteria that developed an ability to tap highly toxic oxygen molecules as a powerful energy source. Eukaryotes lacked this capability, so some of them found a way to swallow the mitochondria's ancestor without digesting it - converting it into an "endosymbiont," an organism that lives within the body of another organism. Unlike the nuclear genome, which is built from a combination of father's and mother's genetic material, the mitochondrial genome is passed down exclusively from the mother. As a result, male offspring are an evolutionary dead end. While natural selection actively suppresses mutations in the mitochondrial DNA (mtDNA) that weaken females, there is no direct mechanism for weeding out those that weaken males: a situation that leads to the mother's curse.
While natural selection actively suppresses mutations in the mitochondrial DNA (mtDNA) that weaken females, there is no direct mechanism for weeding out those that weaken males: the situation that makes the mother's curse possible.
Now, a team of biologists from Vanderbilt University and the Fred Hutchinson Cancer Research Center in Seattle have discovered a mtDNA mutant in the fruit fly Drosophila melanogaster that substantiates the mother's curse hypothesis in animals: It reduces male offspring's fertility as they age but does not have any observable effect on female siblings.
http://phys.org/news/2016-08-discovery-male-harming-dna-mutation-mother.html
Study: https://elifesciences.org/content/5/e16923
Such a possibility arises because there are two independent parts of the genome in the eukaryote cells, which are found in plants and animals, and the two are locked in a "conflict-driven molecular arms race" that impacts human health and wellness. The lion's share of the genome is located in the cell nucleus. But there is also a much smaller secondary portion located in the mitochondria.
According to the generally accepted theory, mitochondria were originally independent bacteria that developed an ability to tap highly toxic oxygen molecules as a powerful energy source. Eukaryotes lacked this capability, so some of them found a way to swallow the mitochondria's ancestor without digesting it - converting it into an "endosymbiont," an organism that lives within the body of another organism. Unlike the nuclear genome, which is built from a combination of father's and mother's genetic material, the mitochondrial genome is passed down exclusively from the mother. As a result, male offspring are an evolutionary dead end. While natural selection actively suppresses mutations in the mitochondrial DNA (mtDNA) that weaken females, there is no direct mechanism for weeding out those that weaken males: a situation that leads to the mother's curse.
While natural selection actively suppresses mutations in the mitochondrial DNA (mtDNA) that weaken females, there is no direct mechanism for weeding out those that weaken males: the situation that makes the mother's curse possible.
Now, a team of biologists from Vanderbilt University and the Fred Hutchinson Cancer Research Center in Seattle have discovered a mtDNA mutant in the fruit fly Drosophila melanogaster that substantiates the mother's curse hypothesis in animals: It reduces male offspring's fertility as they age but does not have any observable effect on female siblings.
http://phys.org/news/2016-08-discovery-male-harming-dna-mutation-mother.html
Study: https://elifesciences.org/content/5/e16923