Abstract:
:We recently demonstrated the requirement of two-pore channel type 2 (TPC2)-mediated Ca2+ release during slow muscle cell differentiation and motor circuit maturation in intact zebrafish embryos. However, the upstream trigger(s) of TPC2/Ca2+ signaling during these developmental processes remains unclear. Nicotinic acid adenine dinucleotide phosphate (NAADP) is a potent Ca2+ mobilizing messenger, which is suggested to target TPC2 in mediating the release of Ca2+ from acidic vesicles. Here, we report the molecular cloning of the zebrafish ADP ribosyl cyclase (ARC) homolog (i.e., ARC1-like), which is a putative enzyme for generating NAADP. We characterized the expression of the arc1-like transcript and the NAADP levels between ~ 16 h post-fertilization (hpf) and ~ 48 hpf in whole zebrafish embryos. We showed that if ARC1-like (when fused with either EGFP or tdTomato) was overexpressed it localized in the plasma membrane, and associated with intracellular organelles, such as the acidic vesicles, Golgi complex and sarcoplasmic reticulum, in primary muscle cell cultures. Morpholino (MO)-mediated knockdown of arc1-like or pharmacological inhibition of ARC1-like (via treatment with nicotinamide), led to an attenuation of Ca2+ signaling and disruption of slow muscle cell development. In addition, the injection of arc1-like mRNA into ARC1-like morphants partially rescued the Ca2+ signals and slow muscle cell development. Together, our data might suggest a link between ARC1-like, NAADP, TPC2 and Ca2+ signaling during zebrafish myogenesis.
journal_name
Dev Bioljournal_title
Developmental biologyauthors
Kelu JJ,Webb SE,Galione A,Miller ALdoi
10.1016/j.ydbio.2018.11.005subject
Has Abstractpub_date
2019-01-15 00:00:00pages
211-225issue
2eissn
0012-1606issn
1095-564Xpii
S0012-1606(18)30508-6journal_volume
445pub_type
杂志文章abstract::The first step in the development of the Drosophila optic medullar primordia is the expansion of symmetrically dividing neuroepithelial cells (NEs); this step is then followed by the appearance of asymmetrically dividing neuroblasts (NBs). However, the mechanisms responsible for the change from NEs to NBs remain uncle...
journal_title:Developmental biology
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journal_title:Developmental biology
pub_type: 杂志文章
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journal_title:Developmental biology
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journal_title:Developmental biology
pub_type: 杂志文章
doi:10.1016/j.ydbio.2012.02.017
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journal_title:Developmental biology
pub_type: 杂志文章,评审
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journal_title:Developmental biology
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journal_title:Developmental biology
pub_type: 杂志文章
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journal_title:Developmental biology
pub_type: 杂志文章
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