Linked Life Data

11161577

Source:http://linkedlifedata.com/resource/pubmed/id/11161577

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pubmed-article:11161577pubmed:abstractTextCa2+ entry during electrical activity plays several critical roles in development. However, the mechanisms that regulate Ca2+ influx during early embryogenesis remain unknown. In ascidians, a primitive chordate, development is rapid and blastomeres of the muscle and neuronal lineages are easily identified, providing a simple model for studying the expression of voltage-dependent Ca2) channels (VDCCs) in cell differentiation. Here we isolate an ascidian cDNA, TuCa1, a homologue of the alpha(1)-subunit of L-type class Ca2+ channels. We unexpectedly found another form of Ca2+ channel cDNA (3-domain-type) potentially encoding a truncated type which lacked the first domain and a part of the second domain. An analysis of genomic sequence suggested that 3-domain-type RNA and the full-length type have alternative transcriptional start sites. The temporal pattern of the amount of 3-domain-type RNA was the reverse of that of the full-length type; the 3-domain type was provided maternally and persisted during early embryogenesis, whereas the full-length type was expressed zygotically in neuronal and muscular lineage cells. Switching of the two forms occurred at a critical stage when VDCC currents appeared in neuronal or muscular blastomeres. To examine the functional roles of the 3-domain type, it was coexpressed with the full-length type in Xenopus oocyte. The 3-domain type did not produce a functional VDCC current, whereas it had a remarkable inhibitory effect on the functional expression of the full-length form. In addition, overexpression of the 3-domain type under the control of the muscle-specific actin promoter in ascidian muscle blastomeres led to a significant decrease in endogenous VDCC currents. These findings raise the possibility that the 3-domain type has some regulatory role in tuning current amplitudes of VDCCs during early development.lld:pubmed
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pubmed-article:11161577pubmed:authorpubmed-author:OkadaTTlld:pubmed
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pubmed-article:11161577pubmed:authorpubmed-author:NakajoKKlld:pubmed
pubmed-article:11161577pubmed:copyrightInfoCopyright 2001 Academic Press.lld:pubmed
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pubmed-article:11161577pubmed:pagination258-77lld:pubmed
pubmed-article:11161577pubmed:dateRevised2003-11-14lld:pubmed
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pubmed-article:11161577pubmed:year2001lld:pubmed
pubmed-article:11161577pubmed:articleTitleThe maternal transcript for truncated voltage-dependent Ca2+ channels in the ascidian embryo: a potential suppressive role in Ca2+ channel expression.lld:pubmed
pubmed-article:11161577pubmed:affiliationIon Channel Group, National Institute of Bioscience and Human Technology, Ibaraki, 305-8566, Japan.lld:pubmed
pubmed-article:11161577pubmed:publicationTypeJournal Articlelld:pubmed
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