Open AccessThe conserved molting/circadian rhythm regulator NHR-23/NR1F1 serves as an essential co-regulator ofC. elegansspermatogenesis
Author(s) -
James Matthew Ragle,
Abigail L. Aita,
Kayleigh N. Morrison,
Raquel Martínez-Méndez,
Hannah N. Saeger,
Guinevere Ashley,
Londen C. Johnson,
Katherine Schubert,
Diane C. Shakes,
Jordan D. Ward
Publication year - 2020
Publication title -
development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.754
H-Index - 325
eISSN - 1477-9129
pISSN - 0950-1991
DOI - 10.1242/dev.193862
Subject(s) - biology , regulator , circadian rhythm , microbiology and biotechnology , spermatogenesis , circadian clock , caenorhabditis elegans , master regulator , moulting , neuroscience , genetics , endocrinology , transcription factor , gene , ecology , larva
In sexually reproducing metazoans, spermatogenesis is the process by which uncommitted germ cells give rise to haploid sperm. Work in model systems has revealed mechanisms controlling commitment to the sperm fate, but how this fate is subsequently executed remains less clear. While studying the well-established role of the conserved nuclear hormone receptor transcription factor, NHR-23/NR1F1, in regulating C. elegans molting, we discovered NHR-23/NR1F1 is also constitutively expressed in developing 1° spermatocytes and is a critical regulator of spermatogenesis. In this novel role, NHR-23/NR1F1 functions downstream of the canonical sex determination pathway. Degron-mediated depletion of NHR-23/NR1F1 within hermaphrodite or male germlines causes sterility due to an absence of functional sperm as depleted animals produce arrested primary spermatocytes rather than haploid sperm. These spermatocytes arrest in prometaphase I and fail to either progress to anaphase or attempt spermatid-residual body partitioning. They make sperm-specific membranous organelles (MOs) but fail to assemble their major sperm protein into fibrous bodies. NHR-23/NR1F1 appears to function independently of the known SPE-44 gene regulatory network, revealing the existence of an NHR-23/NR1F1-mediated module that regulates the spermatogenesis program.