Depletion of gipc-1 and gipc-2 causes infertility in Caenorhabditis elegans by reducing sperm motility

The G-protein signaling pathway plays a key role in multiple cellular processes and is well conserved in eukaryotes. Although GIPC (G-protein a subunit interacting protein (GAIP)-interacting protein, C terminus) has been studied in several model organisms, little is known about its role in Caenorhabditis elegans. In the present study, we investigated the roles of gipc-1 and gipc-2 in C. elegans. We observed that they were exclusively expressed in sperm throughout the development and that gipc-1; gipc-2 double mutants were infertile. Further examination of sperm development in gipc-1; gipc-2 mutants revealed defective sperm activation and abnormal pseudopod extension that resulted in reduced sperm motility. Moreover, major sperm protein (MSP) was abnormally segregated between spermatids and residual bodies in gipc-1; gipc-2 mutants. Our findings indicate that gipc-1 and gipc-2 are required for the proper pseudopod extension of sperm during the terminal differentiation of spermatids. During this process, the segregation of MSP into spermatids is important for ensuring normal sperm motility during fertilization. (C) 2020 Elsevier Inc. All rights reserved.

Automated summary

The GIPC proteins, gipc-1 and gipc-2, are crucial for proper pseudopod extension of sperm in Caenorhabditis elegans, leading to normal sperm motility during fertilization. Their deficiency results in defective sperm activation and abnormal segregation of major sperm protein (MSP), ultimately causing infertility in double mutants.