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The rat Kir7.1 gene spans >40 kb with eight exons, exhibits complex tissue-specific alternative splicing, and is regulated by cAMP through a CCAAT element.
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The study elucidates the complex genomic structure and cAMP-dependent regulation of the rat Kir7.1 potassium channel gene, providing insights into its tissue-specific expression.
Genomic organization of the rat inward rectifier K(+) channel Kir7.1 was determined in an attempt to clarify how multiple species of its mRNA are generated in a tissue-specific manner and how its expression is regulated. The rat Kir7.1 gene spans >40 kilobases (kb) and consists of eight exons; the first four exons encode the 5'-untranslated region that is unusually long ( approximately 3 kb). The coding region is located in exons 5 and 6. In the testis, exon 4 is processed as four exons (4a-4d), whereas it is recognized as a single exon in the small intestine. The three major species of rat Kir7.1 mRNA (1.4, 2.2, and 3.2 kb) were found to arise from alternative usage of the two promoters and polyadenylation signals and by alternative splicing of the 5'-noncoding exons. The splicing pattern of the 5'-noncoding exons is quite complex and highly tissue-specific, suggesting that complex mechanisms may operate to regulate the Kir7.1 expression. Deletion and mutational analysis of the promoter activity indicated that the rat Kir7.1 gene is regulated by cAMP through a CCAAT element. The cAMP induction was also demonstrated using the rat follicular cell line FRTL-5 endogenously expressing Kir7.1.
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Nakamura et al. (2000) studied this question. The rat Kir7.1 gene spans >40 kb with eight exons, exhibits complex tissue-specific alternative splicing, and is regulated by cAMP through a CCAAT element.
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