Source:http://linkedlifedata.com/resource/pubmed/id/11161577
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
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| pubmed:dateCreated |
2001-2-22
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| pubmed:databankReference | |
| pubmed:abstractText |
Ca2+ 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.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels, L-Type,
http://linkedlifedata.com/resource/pubmed/chemical/DNA, Complementary,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins
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| pubmed:status |
MEDLINE
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| pubmed:month |
Feb
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| pubmed:issn |
0012-1606
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| pubmed:author | |
| pubmed:copyrightInfo |
Copyright 2001 Academic Press.
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| pubmed:issnType |
Print
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| pubmed:day |
15
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| pubmed:volume |
230
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
258-77
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| pubmed:dateRevised |
2003-11-14
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| pubmed:meshHeading |
pubmed-meshheading:11161577-Amino Acid Sequence,
pubmed-meshheading:11161577-Animals,
pubmed-meshheading:11161577-Base Sequence,
pubmed-meshheading:11161577-Calcium Channels,
pubmed-meshheading:11161577-Calcium Channels, L-Type,
pubmed-meshheading:11161577-Cloning, Molecular,
pubmed-meshheading:11161577-DNA, Complementary,
pubmed-meshheading:11161577-Embryo, Nonmammalian,
pubmed-meshheading:11161577-Female,
pubmed-meshheading:11161577-Genomic Imprinting,
pubmed-meshheading:11161577-Molecular Sequence Data,
pubmed-meshheading:11161577-Morphogenesis,
pubmed-meshheading:11161577-Muscles,
pubmed-meshheading:11161577-Oocytes,
pubmed-meshheading:11161577-Protein Structure, Secondary,
pubmed-meshheading:11161577-RNA, Messenger,
pubmed-meshheading:11161577-RNA Splicing,
pubmed-meshheading:11161577-Rabbits,
pubmed-meshheading:11161577-Recombinant Proteins,
pubmed-meshheading:11161577-Sequence Alignment,
pubmed-meshheading:11161577-Sequence Homology, Amino Acid,
pubmed-meshheading:11161577-Sequence Homology, Nucleic Acid,
pubmed-meshheading:11161577-Transcription, Genetic,
pubmed-meshheading:11161577-Urochordata,
pubmed-meshheading:11161577-Xenopus laevis
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| pubmed:year |
2001
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| pubmed:articleTitle |
The maternal transcript for truncated voltage-dependent Ca2+ channels in the ascidian embryo: a potential suppressive role in Ca2+ channel expression.
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| pubmed:affiliation |
Ion Channel Group, National Institute of Bioscience and Human Technology, Ibaraki, 305-8566, Japan.
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| pubmed:publicationType |
Journal Article
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