The DSL ligand APX-1 is required for normal ovulation in C. elegans

Developmental biology

Marie McGovern^1,2¹  Laura G. Vallier^4²  Olga Pekar^2³  Perla Gisela Castaneda^3⁴ 

[1] Department of Biological Sciences, Kingsborough Community College, City University of New York, 2001 Oriental Blvd, Brooklyn, NY 11235, United States^1;Department of Biology, Hofstra University, Hempstead, NY 11549, United States^4;Department of Biology, Northeastern University, Boston, MA 02115, United States^3;Skirball Institute of Biomolecular Medicine, Departments of Cell Biology and Pathology, New York University School of Medicine, New York, NY 10016, United States^2

关键词: Somatic gonad;    Emo;    Spermatheca;    Reproduction;    Notch;    LIN-12;   

DOI  :  10.1016/j.ydbio.2018.01.009

学科分类：生物科学（综合）

来源: Academic Press

【 摘 要 】

DSL ligands activate the Notch receptor in many cellular contexts across metazoa to specify cell fate. In addition, Notch receptor activity is implicated in post-mitotic morphogenesis and neuronal function. In C. elegans, the DSL family ligand APX-1 is expressed in a subset of cells of the proximal gonad lineage, where it can act as a latent proliferation-promoting signal to maintain proximal germline tumors. Here we examine apx-1 in the proximal gonad and uncover a role in the maintenance of normal ovulation. Depletion of apx-1 causes an endomitotic oocyte (Emo) phenotype and ovulation defects. We find that lag-2 can substitute for apx-1 in this role, that the ovulation defect is partially suppressed by loss of ipp-5, and that lin-12 depletion causes a similar phenotype. In addition, we find that the ovulation defects are often accompanied by a delay of spermathecal distal neck closure after oocyte entry. Although calcium oscillations occur in the spermatheca, calcium signals are abnormal when the distal neck does not close completely. Moreover, oocytes sometimes cannot properly transit through the spermatheca, leading to fragmentation of oocytes once the neck closes. Finally, abnormal oocytes and neck closure defects are seen occasionally when apx-1 or lin-12 activity is reduced in adult animals, suggesting a possible post-developmental role for APX-1 and LIN-12 signaling in ovulation.

【 授权许可】

CC BY