Human somatic cells and reproductive cells use distinctive organic mechanisms that exhibit a thin line of similarities between the kinds of genes needed to keep oocytes strong and fertile and the genes that extend life expectancy. This is based on the result of a study on human aging conducted by Dr. Coleen Murphy of Princeton University. The distinct genetic trails provide a clearer understanding and verifiable data about why female fertility starts to degenerate beyond 35 years even though somatic cells are not yet showing indicators of aging until a couple of decades later.
In order to show a comparison between the distinct genetic trails for somatic cells and 
oocytes, Murphy examined the specimen C. elegans, the notable nematode that in 1990 was found to undergo changes with its genetic makeup affecting insulin production that extends its lifespan. Similar insulin mechanism trails have also been detected in humans and could be developed for possible human longevity.
Through DNA microarrays, Murphy and her team of researchers measured the expression levels of genes and discovered a particular genetic signature from degenerating oocytes. Then they compared these genetic expressions with the microarray transcription data on C. elegans. They have further discovered that although insulin participates in aging of these cells, the cellular mechanisms to preserve organic function and to fight degeneration are quite different.
Past studies of the Murphy team proved that oocytes of C. elegans survive about half of the worm’s lifespan, a signature that is also notable with human egg cells. The degeneration of C. elegans oocytes is very slow with a lower signaling mechanism in insulin regulation and genetic trails. With the help of the microarray mechanism, the researchers noted the genes of the C. elegans that were being enabled and disabled as oocytes degenerated. It was also revealed that there is a particular genetic expression for degenerating oocytes that is overturned in insulin and beta mutants. Again, these expressions were compared to the data from the experiments using the well-renowned genetic longevity mutations.
Unexpectedly, the genetic trails were not similar. Although both somatic and oocytes are degenerating in C. elegans both using the insulin pathway, the mechanism to preserve organic function and to fight degeneration are very different. Murphy emphasized that searching for ways to slow down the degeneration of reproductive cells could result in the reduction of risks for mature women in giving birth to a child with inherent defects.
Source: American Society for Cell Biology. 8 December 2011.