A New Player in the Spermiogenesis Pathway of Caenorhabditis elegans.
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 SPE-6 and perhaps other proteins, termed "the brake model." Here, we identify the spe-47 gene from the hc198 mutation that causes premature spermiogenesis. The mutation was isolated in a suppressor screen of spe-27(it132ts), which normally renders worms sterile, due to defective transduction of the activation signal. In a spe-27(+) background, spe-47(hc198) causes a temperature-sensitive reduction of fertility, and in addition to premature spermiogenesis, many mutant sperm fail to activate altogether. The hc198 mutation is semidominant, inducing a more severe loss of fertility than do null alleles generated by CRISPR-associated protein 9 (Cas9) technology. The hc198 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 SPE-47 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 SPE-47 reporters dissociate and disappear. SPE-47 reporter localization is not altered by either the hc198 mutation or a C-terminal truncation deleting the MSP domain. The disappearance of SPE-47 reporters prior to the formation of spermatids requires a reevaluation of the brake model for prevention of premature spermatid activation.
Department of Biological Science, California State Polytechnic University, Pomona, California 91768 cwlamunyon@cpp.edu.
Craig W
CW
LaMunyon
Department of Biological Science, California State Polytechnic University, Pomona, California 91768.
Ubaydah
U
Nasri
Department of Biological Science, California State Polytechnic University, Pomona, California 91768.
Nicholas G
NG
Sullivan
Department of Biological Science, California State Polytechnic University, Pomona, California 91768.
Misa A
MA
Shaw
Department of Biological Science, California State Polytechnic University, Pomona, California 91768.
Gaurav
G
Prajapati
Department of Biological Science, California State Polytechnic University, Pomona, California 91768.
Matthew
M
Christensen
Department of Biological Science, California State Polytechnic University, Pomona, California 91768.
Daniel
D
Elmatari
Department of Biological Science, California State Polytechnic University, Pomona, California 91768.
Jessica N
JN
Clark
D000595:Amino Acid Sequence; D000818:Animals; D001483:Base Sequence; D017173:Caenorhabditis elegans / Q000235:genetics*; D029742:Caenorhabditis elegans Proteins / Q000235:genetics*; D002874:Chromosome Mapping; D018509:DNA, Helminth; D017238:Genes, Helminth; D008297:Male; D008969:Molecular Sequence Data; D009154:Mutation; D020641:Polymorphism, Single Nucleotide; D017422:Sequence Analysis, DNA; D013091:Spermatogenesis / Q000235:genetics*; D014170:Transformation, Genetic
D029742:Caenorhabditis elegans Proteins; D018509:DNA, Helminth; C000609908:SPE-47 protein, C elegans
MSP; fibrous body-membranous organelle; spermatogenesis; spermiogenesis