%0 Journal Article
%T The calcium channel ¦Â2 (CACNB2) subunit repertoire in teleosts
%A Alicia M Ebert
%A Catherine A McAnelly
%A Ashok Srinivasan
%A Rachel Mueller
%A David B Garrity
%A Deborah M Garrity
%J BMC Molecular Biology
%D 2008
%I BioMed Central
%R 10.1186/1471-2199-9-38
%X Cloning of two zebrafish ¦Â2 subunit genes (¦Â2.1 and ¦Â2.2) indicated they are membrane-associated guanylate kinase (MAGUK)-family genes. Zebrafish ¦Â2 genes show high conservation with mammals within the SH3 and guanylate kinase domains that comprise the "core" of MAGUK proteins, but ¦Â2.2 is much more divergent in sequence than ¦Â2.1. Alternative splicing occurs at the N-terminus and within the internal HOOK domain. In both ¦Â2 genes, alternative short ATG-containing first exons are separated by some of the largest introns in the genome, suggesting that individual transcript variants could be subject to independent cis-regulatory control. In the Tetraodon nigrovidis and Fugu rubripes genomes, we identified single ¦Â2 subunit gene loci. Comparative analysis of the teleost and human ¦Â2 loci indicates that the short 5' exon sequences are highly conserved. A subset of 5' exons appear to be unique to teleost genomes, while others are shared with mammals. Alternative splicing is temporally and spatially regulated in embryo and adult. Moreover, a different subset of spliced ¦Â2 transcript variants is detected in the embryonic heart compared to the adult.These studies refine our understanding of ¦Â2 subunit diversity arising from alternative splicing, and provide the groundwork for functional analysis of ¦Â2 subunit diversity in the embryonic heart.Voltage-dependent L-type Ca2+ channels (V-LTCC) are essential for the initiation and regulation of excitation-contraction coupling in cardiac muscle. In addition, Ca2+ entry through V-LTCC channels can also serve as a second messenger to modulate regulatory protein kinases, calmodulin and beta-adrenergic responses [3]. Genetic mutation of key Ca2+ homeostasis proteins is frequently associated with defects in both cardiac cell differentiation and contractility, suggesting Ca2+ signaling is essential for normal cardiac development [4-7]. Ca2+ signals can also contribute to the control of gene expression [8]. Ca2+ influx through V-LTCC can
%U http://www.biomedcentral.com/1471-2199/9/38