Good contractions: Actomyosin regulation in the C. elegans gonad

Distinct actomyosin structures power a variety of cellular and multicellular processes requiring force. Yet, how actomyosin is regulated in vivo is still poorly understood. We are addressing this question in the model organism C. elegans, and in my talk, I will discuss actomyosin structures related to two parts of its reproductive system: the syncytial germline and the spermatheca. Syncytial architecture is an evolutionary-conserved feature of the germline across species, which plays a crucial role in organism fertility. Our results uncover a novel role for actomyosin contractility in maintaining the architecture of the syncytial germline, and implicate the formin CYK-1 and actin cross-linking protein PLST-1 in its regulation. The spermatheca, a pouch-like myoepithelial tissue, is the site of oocyte ovulation and fertilization, and its contractility is required for transit of the fertilized egg into the uterus. Oocyte entry into the spermatheca triggers its contraction through calcium signalling and the RHO-1-ROCK pathway. We discovered the RhoGAP and GEFs that activates RHO-1 in the spermatheca and found that they are responsive to stretching of the spermatheca by incoming oocytes, thus elucidating a mechanotransduction feedback loop that guarantees the right amount and timing of actomyosin contractility. In summary, our work on C. elegans reproduction is revealing novel mechanisms of molecular control over actomyosin contractility in vivo.