作者: Craig W. LaMunyon , Ubaydah Nasri , Nicholas G. Sullivan , Misa A. Shaw , Gaurav Prajapati
DOI: 10.1534/GENETICS.115.181172
关键词:
摘要: Precise timing of sperm activation ensures the greatest likelihood fertilization. Precision in Caenorhabditis elegans is ensured by external signaling, which induces spherical spermatid to reorganize and extend a pseudopod for motility. Spermatid activation, also called spermiogenesis, prevented from occurring prematurely activity SPE-6 perhaps other proteins, termed "the brake model." Here, we identify spe-47 gene hc198 mutation that causes premature spermiogenesis. The was isolated suppressor screen spe-27(it132ts), normally renders worms sterile, due defective transduction signal. In spe-27(+) background, spe-47(hc198) temperature-sensitive reduction fertility, addition many mutant fail activate altogether. semidominant, inducing more severe loss fertility than do null alleles generated CRISPR-associated protein 9 (Cas9) technology. affects an major (MSP) domain, altering conserved amino acid residue β-strand mediates MSP-MSP dimerization. Both N- C-terminal SPE-47 reporters associate with forming fibrous body (FB)-membranous organelle, specialized organelle packages MSP components during spermatogenesis. Once FB fully formed, dissociate disappear. reporter localization not altered either or truncation deleting domain. disappearance prior formation spermatids requires reevaluation model prevention activation.