Researcher ORCID Identifier

Organization identifiers

ORCID id: 0009-0005-1208-4701 ROR: https://ror.org/04n1me355 Claremont McKenna College: Claremont, California, US

Graduation Year

2026

Date of Submission

4-2026

Document Type

Open Access Senior Thesis

Degree Name

Bachelor of Arts

Department

Molecular Biology

Second Department

Biology

Reader 1

Patrick M. Ferree

Reader 2

Kyle Jay

Rights Information

© 2026 Jacqueline R Solomon

Abstract

Paternal Sex Ratio (PSR) is a supernumerary, selfish B chromosome found in the jewel wasp (Nasonia vitripennis). PSR is transmitted strictly paternally to progeny, and when present, it causes paternal genome elimination (PGE) just after fertilization. Due to the haplo-diploid reproduction of N. vitripennis, this PGE event results in all-male broods of progeny, ~90% of which carry and transmit PSR. Thus, PGE is beneficial for PSR’s transmission.  A previous study showed that PSR induces PGE by expressing a gene called haploidizer during spermatogenesis. Although how haploidizer functions in PGE is unknown, this finding suggests two basic models: that (i) the primary disruption of chromatin occurs during spermatogenesis, perhaps when histones are removed and the sperm’s DNA is packaged with sperm nuclear basic proteins (SNBPs) like protamines, or (ii) the product of haploidizer is transmitted with the sperm into the egg, where the alteration occurs. In this thesis, I have conducted experiments to distinguish between these options. By using immuno-reagents and confocal microscopy, I found that histones are properly removed from the sperm’s DNA during the histone-to-protamine transition. However, using antibodies that detect levels of DNA exposure, I observed a striking difference between wild type and PSR+ sperm: in the latter cell type, the DNA is significantly less exposed when compared to DNA in wild type sperm. This finding, first and foremost, demonstrates a profound difference in chromatin state of developing sperm caused by PSR. Thus, my results strongly argue that PSR’s PGE activity disrupts the sperm’s chromatin during spermatogenesis. More specifically, my findings suggest the possibility that the PGE activity disrupts not histone removal but SNBP loading or ordering during this transition. These findings reveal a new avenue to explore how selfish genetic elements, such as PSR, alter genetic processes to promote their own inheritance.

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