701A Poster - 11. Cell division and cell growth
Thursday April 07, 2:00 PM - 4:00 PM

Authors:
Kaylah Samuelson; Stacey Hanlon

Affiliation: Department of Molecular and Cell Biology, University of Connecticut, Storrs, CT

Keywords:
b. meiosis; c. meiosis

The genome is constantly under attack by selfish genetic elements that bias their transmission to the next generation. A classic type of selfish element B chromosomes - supernumerary, nonessential chromosomes that can be detrimental to their host- were recently discovered in a single laboratory stock of D. melanogaster that carries a null mutation in matrimony (mtrm¹²⁶) held over a third chromosome balancer (TM3, Sb Ser). This combination allows the B chromosomes to be transmitted through female meiosis at a higher-than-expected frequency, a phenomenon referred to as meiotic drive. Though it is clear that having only one functional copy of mtrm is necessary but not sufficient for this drive, the mechanism by which a reduction in Mtrm protein leads to drive of the B chromosomes is unknown. Mtrm has a critical function during female meiosis where it regulates Polo kinase (Polo) to promote centromeric cohesion of achiasmate (non-crossover) chromosomes and ensure their proper segregation during the meiotic divisions. This regulation requires Mtrm to bind to Polo through a highly conserved ST/P domain on Mtrm. One residue, T40, is particularly important for this interaction, as expression of a transgenic copy of Mtrm that has single amino acid change at that position (mtrm^T40A) is unable to rescue defects in the segregation of achiasmate chromosomes in a mtrm¹²⁶ heterozygote. Since Mtrm’s interaction with Polo is necessary to promote the proper segregation of achiasmate chromosomes, I hypothesize that this interaction may also be essential for Mtrm’s ability to suppress the drive of the B chromosomes. To address this hypothesis, we will compare B chromosome transmission frequencies in a drive-competent (mtrm¹²⁶/TM3, Sb Ser) genetic background both in the presence and absence of Mtrm transgenes that affect Mtrm’s ability to bind Polo (e.g., mtrm^T40A). Our investigation will determine if Mtrm’s interaction with Polo is critical for the suppression of B chromosome meiotic drive, indicating that Mtrm’s role in drive suppression and achiasmate chromosome segregation may be mechanistically similar. If the Mtrm-Polo interaction is not required for suppressing B chromosome meiotic drive, this result would lead us to test the necessity of other conserved Mtrm domains in its role as a drive suppressor. Overall, our work is uncovering the genetic mechanisms behind how the host genome protects itself against the proliferation of selfish genetic elements.