The DSL ligand APX-1 is required for normal ovulation in C. elegans.
The DSL ligand APX-1 is required for normal ovulation in C. elegans.
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DOI:
10.1016/j.ydbio.2018.01.009
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发表时间:
2018-03-15
影响因子:
2.7
通讯作者:
Hubbard EJA
中科院分区:
文献类型:
--
作者:
McGovern M;Castaneda PG;Pekar O;Vallier LG;Cram EJ;Hubbard EJA
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.
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影响因子:
4.5
作者:
Kovacevic I;Orozco JM;Cram EJ
通讯作者:
Cram EJ
影响因子:
2.4
作者:
Chao MY;Larkins-Ford J;Tucey TM;Hart AC
通讯作者:
Hart AC
DOI:
10.1083/jcb.134.3.699
发表时间:
1996-08
期刊:
The Journal of cell biology
影响因子:
--
作者:
Iwasaki K;McCarter J;Francis R;Schedl T
通讯作者:
Schedl T
影响因子:
7.7
作者:
Li P;Collins KM;Koelle MR;Shen K
通讯作者:
Shen K
影响因子:
56.9
作者:
Miller, MA;Nguyen, VQ;Greenstein, D
通讯作者:
Greenstein, D