Abstract
G protein signaling regulates Ca (2+) dynamics and contractility in the C. elegans spermatheca. G protein-coupled receptors activate heterotrimeric G proteins, triggering downstream cascades, including the Gαs-mediated activation of adenylyl cyclase and subsequent Protein Kinase A (PKA) activation. Our previous work identified GSA-1 /Gαs and PKA as key modulators of Ca²⁺ oscillations and tissue contractility in the C. elegans spermatheca. In this study, we show that the inhibitory Gαi/o subunit GOA-1 regulates spermathecal transit. We employed TurboID proximity labeling and mass spectrometry to identify 16 candidate interactors of GOA-1 . Depletion of these candidates by RNAi did not yield overt spermathecal transit defects.