But those that were present at a higher proportion in the mother were more likely to get passed on, and in some cases may persist for up to five to ten generations. To accomplish this study, the research team relied on a collaboration with co-author Dr. Hershey Medical Center, who oversaw sample collection from individuals in 96 multi-generational families.
Families included at least two siblings, their mother, and in some cases the mother's mother and additional generations. Because the team studied mothers and multiple children in each family, they were able to infer when during oogenesis this bottleneck occurs. If the bottleneck occurs before cells split into separate lineages that will eventually become the eggs that make each child, then siblings should have a similar composition of mitochondrial DNA--the same seven to ten copies of mitochondrial DNA that made it through the bottleneck.
If the bottleneck instead occurs after these lineages have separated--with each lineage independently reducing the amount of DNA during the bottleneck--then siblings should have very different compositions of mitochondrial DNA, which is what the researchers found.
Now that we know when the bottleneck occurs, we hope to investigate oogenesis at a molecular level in animal models to get a better understanding of the process. The study also suggests that egg precursor cells with high proportions of disease-causing mutations might not make it to the next generation because of the evolutionary process called natural selection.
Importantly, children born to mothers that gave birth later in life had more mutation-carrying copies of their mitochondrial DNA as compared to younger mothers.
Cellular DNA, the genetic blueprint that codes for all the proteins in the body, is inherited from both the mother and father. Mitochondrial DNA, however, was believed to only be passed down from the mother. The authors examined the mtDNA of a young patient suspected to have a mitochondrial disorder.
Continuing this analysis in the parents of the maternal grandfather showed a similar biparental inheritance pattern. The sequencing was repeated at two other independent labs, since contamination could have caused these unexpected results.
Two other, unrelated families with high levels of variation in their mtDNA were analyzed and in these families, there is clear evidence for inheritance of mtDNA from both parents as well. The potential implications of this study are far-reaching. Any previous DNA sequence analysis yielding similar results was commonly assumed to be due to contamination or sample mix-up.
It is possible that paternal inheritance of mtDNA is more widespread than even the results of this study suggest. From a biological standpoint, the mechanism underlying this inheritance pattern is completely unknown, and could be due to mutations in mtDNA, cellular DNA, or both.
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Where are these genes found, and how does this non-nuclear inheritance occur? Aa Aa Aa. Uniparental Modes of Inheritance. Figure 1: Experiments by Carl Correns introduced concepts of non-nuclear chromosomal inheritance.
The progeny displayed the same color leaves as the seed plant, regardless of the leaf pattern exhibited by the pollinating plant.
The ratio of these phenotypes did not conform to the phenotypic ratio predicted by Mendelian inheritance laws.
Genetics: A Conceptual Approach , 2nd ed. All rights reserved. Figure Detail. How Uniparental Inheritance Works. Nonnuclear Inheritance and Mendelian Patterns. Biparental Inheritance. Mitochondrial Inheritance. Figure 2: Cytoplasmically inherited characteristics frequently exhibit extensive phenotypic variation because cells and individual offspring contain various proportions of cytoplasmic genes.
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