Key result
Transgenes tni-3 and tni-4 fail to rescue C. elegans motility defects unlike tni-1 and tni-2.
Why the study?
Transcription control of multiple genes in tissue- and stage-specific patterns remains a major interest, particularly for understanding gene evolution and developmental programs.
The tni-3 gene in C. elegans acts as an intermediate isoform between pharynx and body-wall muscle, providing insights into gene evolution and developmental programs.
Indicates non-redundant troponin isoform roles in muscle; leaves open relevance to human cardiac genetics.
Transcription control of multiple genes in tissue- and stage-specific patterns is still of major interest. We show here that troponin I (TNI) is expressed under the control of upstream non-coding sequences and had functions as an isoform of intermediate type between pharynx and body-wall of the gene. In Caenorhabditis elegans, three striated muscle TNIs are expressed in body-wall muscles and a cardiac isoform is expressed in the pharynx. We have analyzed the gene expression mechanisms of tni-3 gene and motility function of its protein product. Promoter deletion analysis of the tni-3 gene identified muscle enhancers including the head enhancer. The CBF1/Su(H)/LAG-1-binding motif was included in the head enhancer. Yeast one-hybrid screening isolated the lag-1 clone in five candidates. Functional differences between the three striated muscle TNIs were investigated by the expression of promoter-fusion genes into tni-2/unc-27(e155) null mutant animals. The results suggest that the cis-elements in the promoters of the three genes are important for their tissue-specific expression and that from the function of TNI-3, the tni-3 gene would be an intermediate in the evolution of these genes by gene duplication. Mechanisms of tni-3 expression and its molecular function may contribute to our understanding of gene evolution and developmental programs.
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Takashima et al. (2012) studied Muscle development and motility. tni-3 transgene expression vs. unc-27(e155) null mutant animals was evaluated on Motility recovery (waving rate compared to wild-type). In C. elegans, tni-3 and tni-4 transgenes failed to rescue motility defects in unc-27 null mutants, unlike tni-1 and tni-2 which significantly restored motility.
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