Date Approved

1-12-2026

Embargo Period

1-12-2026

Document Type

Dissertation

Degree Name

Ph.D. Molecular Cell Biology & Neuroscience

Department

Cell and Molecular Biology

College

Rowan-Virtua School of Translational Biomedical Engineering & Sciences

Advisor

Ronald Ellis, Ph.D.

Committee Member 1

Katrina Cooper, DPhil

Committee Member 2

Michael Henry, Ph.D.

Committee Member 3

Benjamin Rood, Ph.D.

Committee Member 4

Eric Haag, Ph.d.

Keywords

Caenorhabditis;CRISPR;genetic mutation;sex-determination

Disciplines

Genetics | Genetics and Genomics | Life Sciences

Abstract

The Caenorhabditis genus produced three independently-evolved hermaphroditic species, C. elegans, C. briggsae, and C. tropicalis. This convergence happened by the independent co-option of male programs for use in a female body. This required two distinct steps: (1) mutations in the sex-determination pathway that activated spermatogenesis in XX animals, and (2) mutations that expressed one of the redundant sperm activation signals in XX animals. My project focused on characterizing how sex-determination genes work in C. briggsae and C. tropicalis. Loss-of-function alleles were used to compare the core sex-determination pathway to that of C. elegans. I found that the somatic sex-determination pathway is highly conserved in C. tropicalis. However, I detected intriguing differences in how this pathway regulates somatic tissues like the male nervous system and male tail. Germ line sex-determination, while ultimately controlling gamete fates through FOG-3/FOG-1 repression of oogenesis, has seen more significant changes. One conserved aspect of the pathway is that the FEM-1, FEM-2, and FEM-3 proteins appear to act as a complex to regulate TRA-1 degradation in all three species. However, they have a second function downstream of TRA-1 that has changed significantly, and FEM-2 plays little role in this second function in C. tropicalis and C. briggsae. Finally, analysis of C. tropicalis confirms the hypothesis that regulation of TRA-2 is the most sensitive point for altering the control of germ cell fates in XX animals, to allow spermatogenesis.

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