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Colloquium Seminar Series: Mia Levine, University of Pennsylvania | Biological Sciences

Sep 14, 2017
4:10 PM - 5:00 PM

Iacocca Hall - B-023
111 Research Drive
Bethlehem PA 18015

Delia Chatlani

Dr. Mia Levine, Department of Biology and Epigenetics Institute, University of Pennsylvania. Intra-genomic conflict drives evolutionary diversification of DNA packaging proteins 

An individual genome appears to be a cohesive community of distinct genetic elements with common incentives: across developmental time, distinct genetic elements collaborate to build a robust and fertile individual; across evolutionary time, these elements accumulate adaptive mutations that confer yet additional robustness and fertility. However, these contributions to the common good are incidental—each genetic element actually evolves to maximize its own representation in the next generation. Our genome’s sizable fraction of selfish DNA, whose self-perpetuation inflicts a fitness cost, illuminates this paradox. Like the collateral damage of a virus hijacking our cellular machinery for its own replication, these selfish genetic elements compromise genomic integrity when they exploit DNA replication and transmission machinery to increase in frequency in the next generation. Some selfish “mobile elements” copy and paste themselves around the genome haphazardly, compromising genes and gene regulatory information where they insert themselves. Other selfish elements subvert Mendel’s Laws of chromosomal transmission, attaining preferential inclusion into the egg or sperm but ultimately compromising fertility. When these selfish elements win, the rest of the genome loses. Compromised Darwinian fitness puts evolutionary pressure on the genome to police these elements, perpetuating an intra-genomic “molecular arms race”. The Levine lab seeks to define the identity, molecular mechanisms, and biological consequences of the ongoing conflict between genome hijackers and genome guardians. This talk will describe our nascent efforts to address these outstanding problems by genetically manipulating fast-evolving DNA packaging proteins required for either telomere integrity or sex chromosome transmission in the model fruit fly, Drosophila melanogaster.

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