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

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...

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Published in:	Developmental biology Vol. 435; no. 2; pp. 162 - 169
Main Authors:	McGovern, Marie, Castaneda, Perla Gisela, Pekar, Olga, Vallier, Laura G., Cram, Erin J., Hubbard, E. Jane Albert
Format:	Journal Article
Language:	English
Published:	United States Elsevier Inc 15-03-2018
Subjects:	Animal Structures - abnormalities Animal Structures - physiology Animals Caenorhabditis elegans - genetics Caenorhabditis elegans - physiology Caenorhabditis elegans Proteins - genetics Caenorhabditis elegans Proteins - physiology Calcium Signaling Emo Endoreduplication - genetics Hermaphroditic Organisms - genetics Hermaphroditic Organisms - physiology LIN-12 Membrane Proteins - physiology Mitosis Notch Oocytes Ovulation - genetics Ovulation - physiology Phenotype Receptors, Notch - deficiency Receptors, Notch - physiology Reproduction Sodium Channels - deficiency Sodium Channels - genetics Sodium Channels - physiology Somatic gonad Spermatheca Somatic gonad Reproduction LIN-12 Spermatheca Emo Notch
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Summary:	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. •The DSL ligand apx-1 is required for normal ovulation.•Ovulation defects include distal spermathecal neck closure delay after oocyte entry.•Oocyte fragmentation and abnormal calcium signals accompany neck closure defects.•Similar phenotypes are observed upon apx-1 depletion in adults.•Results support a possible post-developmental role for apx-1 in ovulation.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0012-1606 1095-564X
DOI:	10.1016/j.ydbio.2018.01.009