Year: 2026
Type: preprint
Abstract: In the C. elegans reproductive system, oocyte transit through the spermatheca relies on parallel calcium and Rho-dependent signaling pathways to regulate actomyosin contractility. Here, we identify the conserved single-PDZ domain protein TXBP-3/TAX1BP3 as a dosage-dependent regulator of spermathecal contractility. TXBP-3 is expressed in contractile tissues, including the spermatheca and spermathecal-uterine (sp-ut) valve. Animals lacking txbp-3 do not display overt phenotypes or defects in ovulation. However, in nematodes expressing the genetically encoded Ca 2+ sensor GCaMP, deletion of txbp-3 results in more rapid transit of embryos through the spermatheca. Conversely, tissue-specific overexpression of TXBP-3 results in slower transit times due to hypercontraction of the spermathecal neck and sp-ut valve, causing oocyte severing and failures of embryos to exit the spermatheca. We find TXBP-3 promotes the active phosphorylated state of the Ca 2+ /calmodulin-dependent protein kinase II (CaMKII) UNC-43. When TXBP-3 is overexpressed or unc-43 is depleted, ovulations in which the embryo fails to exit show disrupted Ca 2+ signaling. Additionally, TXBP-3 functions independently of the RhoGEF RHGF-1 and in parallel with the RhoGAP SPV-1 to maintain the alignment of actin fiber bundles and protect embryo structural integrity. Together, our results establish TXBP-3 as a regulator of contractility, kinase activation, and cytoskeletal architecture in contractile tissues.
Authors: Maria Khalid, Erin J. Cram
Institution: Northeastern University
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W7220704554