Date of Award

2-1-2025

Publication Type

Thesis

Degree Name

M.Sc.

Department

Biological Sciences

Keywords

Meiosis; PLK4

Supervisor

John Hudson

Rights

info:eu-repo/semantics/openAccess

Abstract

Nearly a tenth of couples struggle with infertility and of these cases half the issues are contributed by the males. Despite continued research, about a third of the cases of male infertility are idiopathic1. Thus, the genetic origin of male infertility requires continued investigation. Given this context, researchers can follow several paths towards uncovering the possible genetic origins for infertility. One such path is the genetic status of cell cycle regulators expressed in the meiotic niche. This has led our lab to the investigation of polo-like kinase 4 (PLK4) as a possible genetic cause for infertility. PLK4 is responsible for the duplication of centrioles, a critical component of the structure of fully developed spermatozoa. We employed a PLK4 heterozygous mouse model for the investigation of PLK4 as a potential genetic origin for the disruption of meiosis2. While we have not found evidence that PLK heterozygosity leads to infertility, there is a statistically significant difference in one proliferative marker when compared between the heterozygous and the wild-type population and a difference in the expression pattern of PLK4 when observed in immunohistochemistry. The amount of PLK4 protein was also quantified through Western blot analysis and immunohistochemistry, and several other markers of cells in the testes were used to attempt to characterize the reproductive health of the seminiferous epithelium on a more granular scale than with simple morphological analysis. The results of many of these markers was found to be inconclusive. We believe that this work sets a foundation for further investigation of the meiotic niche via immunohistochemistry.

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