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Regulation of α1G T‐type calcium channel gene (CACNA1G) expression during neuronal differentiation
Author(s) -
Bertolesi Gabriel E.,
Jollimore Christine A. B.,
Shi Chanjuan,
Elbaum Lindsy,
DenovanWright Eileen M.,
Barnes Steven,
Kelly Melanie E. M.
Publication year - 2003
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.2003.02618.x
Subject(s) - repressor , promoter , biology , enhancer , microbiology and biotechnology , gene , gene expression , regulation of gene expression , cellular differentiation , transcription (linguistics) , regulatory sequence , genetics , linguistics , philosophy
Down‐regulation of T‐type Ca channel current and mRNA occurs following differentiation of Y79 retinoblastoma cells. To understand how the decrease in expression is linked to cell differentiation, we examined transcriptional regulation of the Ca v 3.1 Ca channel gene, CACNA1G. We identified two putative promoters (A and B) in 1.3 kb of cloned genomic DNA. Reverse transcriptase‐polymerase chain reaction and 5′ rapid amplification of cDNA ends‐polymerase chain reaction analyses demonstrated that two transcripts with different 5′ untranslated regions are generated by different transcription start sites, with promoter A favoured in undifferentiated cells and promoter B favoured in differentiated cells. Functional analyses of the promoter sequence revealed that both promoters are active. Enhancer and repressor sequences were identified upstream of promoter A and B, respectively. These results suggest that the down‐regulation of α1G mRNA in differentiated Y79 cells is mediated primarily by decreased activity of promoter A, which could occur in conjunction with repression of the activity of promoter B. The decrease in T‐type Ca channel expression in Y79 cells may be an essential signal affecting phenotypic maturation and expression of other ion channel subtypes in the differentiated cells.