A New Player in the Spermiogenesis Pathway of Caenorhabditis elegans

摘要

Precise timing of sperm activation ensures the greatest likelihood of fertilization. Precision in Caenorhabditis elegans sperm activation is ensured by external signaling, which induces the spherical spermatid to reorganize and extend a pseudopod for motility. Spermatid activation, also called spermiogenesis, is prevented from occurring prematurely by the activity of and perhaps other proteins, termed “the brake model.” Here, we identify the gene from the mutation that causes premature spermiogenesis. The mutation was isolated in a suppressor screen of (), which normally renders worms sterile, due to defective transduction of the activation signal. In a (+) background, () causes a temperature-sensitive reduction of fertility, and in addition to premature spermiogenesis, many mutant sperm fail to activate altogether. The mutation is semidominant, inducing a more severe loss of fertility than do null alleles generated by CRISPR-associated protein 9 (Cas9) technology. The mutation affects an major sperm protein (MSP) domain, altering a conserved amino acid residue in a β-strand that mediates MSP–MSP dimerization. Both N- and C-terminal reporters associate with the forming fibrous body (FB)-membranous organelle, a specialized sperm organelle that packages MSP and other components during spermatogenesis. Once the FB is fully formed, the reporters dissociate and disappear. reporter localization is not altered by either the mutation or a C-terminal truncation deleting the MSP domain. The disappearance of reporters prior to the formation of spermatids requires a reevaluation of the brake model for prevention of premature spermatid activation.