Key result
A 300-bp minimal promoter containing intact GATA and CArG-box elements from the amphibian TnIc gene is sufficient to drive reporter gene expression mimicking the endogenous Xenopus TnIc gene.
Amphibian cardiac troponin I gene regulation differs from mammals, relying on a 300-bp minimal promoter with GATA and CArG-box elements rather than thyroid hormone.
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Defines compact amphibian TnIc promoter elements; leaves open relevance to mammalian cardiac gene regulation or therapy.
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.
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Warkman et al. (2003) studied this question. 5'-flanking region of Rana catesbeiana TnIc gene was evaluated on Expression of green fluorescent protein in Xenopus transgenic system. A 300-bp minimal promoter containing intact GATA and CArG-box elements from the amphibian TnIc gene is sufficient to drive reporter gene expression mimicking the endogenous Xenopus TnIc gene.
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