Premature Sperm Activation and Defective Spermatogenesis Caused by Loss of spe-46 Function in Caenorhabditis elegans

摘要: Given limited resources for motility, sperm cell activation must be precisely timed to ensure the greatest likelihood of fertilization. Like those most species, C. elegans become active only after encountering an external signaling molecule. Activation coincides with spermiogenesis, final step in spermatogenesis, when spherical spermatid undergoes wholesale reorganization produce a pseudopod. Here, we describe gene involved activation, spe-46. This was identified suppressor screen spe-27(it132ts), sperm-expressed whose product functions transduction signal. While spe-27(it132ts) worms are sterile at 25°C, spe-46(hc197)I; spe-27(it132ts)IV double mutants regain partial fertility. Single nucleotide polymorphism mapping, whole genome sequencing, and transformation rescue were employed identify spe-46 coding sequence. It encodes protein seven predicted transmembrane domains but no other functional or homology outside nematodes. Expression is spermatogenic tissue, transcriptional GFP fusion shows expression corresponds onset pachytene stage meiosis. The spe-46(hc197) mutation bypasses need signal; mutant activate prematurely without signal males, males sterile. In otherwise wild-type genome, induces defective phenotype. addition premature exhibit numerous defects including aneuploidy, vacuolization, protruding spikes, precocious membranous organelles. Hemizygous [spe-46(hc197)/mnDf111] effectively Thus, appears regulation during null phenotype being absence hypomorphic phenotypes defects.