Amphibian cardiac troponin I gene's organization, developmental expression, and regulatory properties are different from its mammalian homologue.

Abstract

In mammals, the expression of the troponin I-slow (TnIs) isoform is predominant in the heart during embryogenesis and, shortly after birth, is replaced by the cardiac-specific isoform, TnIc; a developmental switch thought to be mediated by thyroid hormone. Whereas, in Xenopus, TnIc is expressed at the onset of heart formation and is the only TnI isoform expressed in the heart. Herein, we demonstrate that the expression patterns of these genes appear to be common within the anuran lineage and, unlike their mammalian counterparts, are not affected by thyroid hormone. To elucidate the regulatory mechanism(s) governing the expression of the amphibian TnIc gene, we characterized the TnIc gene from Rana catesbeiana and used its 5'-flanking region to drive expression of green fluorescent protein in the Xenopus transgenic system. Our results demonstrate that a 300-bp minimal promoter containing intact GATA and CArG-box elements is sufficient to drive expression of this reporter gene in a pattern that mimics, both spatially and temporally, the expression of the endogenous Xenopus TnIc gene.