GOA-1 regulates spermathecal transits

G protein signaling regulates Ca <sup>2+</sup> dynamics and contractility in the <i>C. elegans</i> 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 <i>C. elegans</i> 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.

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Publication Details

Journal
PubMed
Published
2025-09-30
DOI
https://doi.org/10.17912/micropub.biology.001877
Citations
1
Primary Topic
Cellular transport and secretion
Type
article
Field-Weighted Citation Impact
1.15
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article

GOA-1 regulates spermathecal transits

Virginie Sjoelund, Erin J. Cram, Fereshteh Sadeghian
1 citations
PubMed
Cellular transport and secretion
1.15
article

GOA-1 regulates spermathecal transits

Virginie Sjoelund, Erin J. Cram, Fereshteh Sadeghian
article en
1 citations

Abstract

G protein signaling regulates Ca <sup>2+</sup> dynamics and contractility in the <i>C. elegans</i> 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 <i>C. elegans</i> 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.

PubMedVol. 2025
Northeastern University (US)
Openalex Percentile: Top 17%
Cellular transport and secretion
1.15
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