Researcher ORCID Identifier

0000-0003-0412-1339

Graduation Year

2022

Document Type

Campus Only Senior Thesis

Degree Name

Bachelor of Arts

Department

Biology

Reader 1

Patrick Ferree

Reader 2

Findley Finseth

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Terms of Use for work posted in Scholarship@Claremont.

Rights Information

2022 Salina M Teklay

Abstract

Supernumerary, B, chromosomes are selfish genetic elements that manipulate mitosis and meiosis to prioritize their proliferation over the fitness and survival of their host genome. One of the most deleterious examples of this is the B chromosome Paternal Sex Ratio (PSR) distorter in Nasonia vitripennis, the jewel wasp. PSR, a paternal chromosome, disrupts the chromatin structure of the paternal genome and causes female-destined diploid embryos to turn into haploid male embryos. PSR is known to do this by causing an enrichment of histone post-translational modifications during the first mitosis which causes the paternal chromatin to not form into individualized chromosomes and instead form the Paternal Chromatin Mass (PCM). My work studied how PSR was able to evade these harmful effects despite being present in the sperm’s nucleus at the time of paternal genome elimination (PGE). Due to the similarities between PSR and heterochromatin, I decided to stain the PCM for heterochromatic sequences, specifically rDNA and satellite DNA, to see if they, too, were unaffected by PSR’s histone enrichment. rDNA failed to be marked by H3K9me2,3 and H4K20me1 which supports my theory that PSR shares qualities of heterochromatin which may help it to survive PGE. Future studies still need to be done to definitively make comparisons between the two genetic elements, but this is a step closer to uncovering PSR’s means of protection.

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