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Bortvin's group had previously demonstrated that jumping genes are quashed during sperm production, but not during egg development. They theorized that purging the cells with the greatest activity by the jumping gene LINE-1 allows for the selective survival of the immature eggs that have the lowest potential of succumbing to jumping genes.
Indeed, Malki and Bortvin previously discovered that AZT, a drug that blocks the multiplication of HIV and LINE-1, temporarily prevented death of immature egg cells. This observation indicated that that there was more than one mechanism to detect and eliminate egg cells with excessive LINE-1 activity.
Taking this idea to the next stage, the research team expanded their investigations by using AZT in mice lacking a protein called Chk2, which detects DNA damage and either repairs it or flags the cells where this genetic material is housed for death. When the LINE-1 jumping gene was inhibited by AZT, and the Chk2 protein was rendered ineffective by mutation, the reserve of egg cells increased.
"What's more, the shutting off the fetal egg cell elimination process in this way did not decrease fertility," Tharp explained. "This provides further evidence that this is a quality control process undertaken to try to maintain the caliber of the available egg supply."
More work is needed to determine whether these findings could help combat infertility due to premature ovarian failure by increasing a woman's total egg supply. Source:
Carnegie Institution for Science Journal reference:
Tharp, M. E., et al. (2020) Maximizing the ovarian reserve in mice by evading LINE-1 genotoxicity. Nature Communications . doi.org/10.1038/s41467-019-14055-8 .
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