536A Poster - 07. Chromatin, epigenetics and genomics
Thursday April 07, 2:00 PM - 4:00 PM

Unique chromatin characteristics allow a genome-eliminating B chromosome to avoid self-elimination


Authors:
Salina Teklay 1; Haena Lee 1,3; Pooreum Seo 1; Emily Yuguchi 1; Elena Dalla Benetta 1,3; John Werren 2; Patrick Ferree 1

Affiliations:
1) Claremont Colleges, Claremont, CA; 2) University of Rochester, Rochester, NY; 3) UC San Diego, San Diego, CA

Keywords:
a. chromatin structure; r. other (early embryogenesis)

Insects harbor a wide array of reproductive parasites, including selfish B chromosomes. One of the most dramatic examples is a B chromosome known as PSR (for Paternal Sex Ratio), which resides in natural populations of the jewel wasp, Nasonia vitripennis. PSR is paternally transmitted via the sperm’s nucleus to progeny, and it causes complete destruction of the sperm’s hereditary material, but not itself, during the first embryonic mitotic division. This action converts female-destined embryos into haploid males, which can then transmit PSR. A compelling question is how PSR escapes its own genome-eliminating activity. We previously found that while PSR causes heightened H3K27me1 and H4K20me1 across the paternal genome just before it is eliminated, PSR itself does not incur these marks. Here we have found that the segregation of PSR is only partially affected by the CI activity of Wolbachia. While Wolbachia like PSR causes heightened H3K27me1 and H4K20mel across the paternal genome, PSR remains unmarked regarding these histone modifications in the presence of this chromatin-altering bacterium. These findings suggest that PSR’s chromatin exhibits unique properties compared to the essential genome complement. We hypothesized that PSR may not participate in the histone-to-protamine transition as a way of evading chromatin disruption. However, this idea was not supported; when the histone chaperone HIRA was knocked down by systemic RNAi, PSR completely failed to segregate. Our current efforts are aimed at examining other chromatin-related characteristics to explain PSR’s intriguing ability to escape its own genome eliminating activity.