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Control mechanisms of transcription factors of muscle gene expressions in Caenorhabditis elegans Export

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C. elegans / WormBase's tags for this article

b03041 c33d31 caenorhabditis_elegans celegans c_elegans elegans elt-2 f38a61 hlh-1 lev-11 meeting_abstract nematode pha-4 wormbase y105e8b1

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" We present two results of transcription factors controlling the tropomyosin and CeMyoD genes expressions. The single tropomyosin gene of C. elegans, tmy-1/lev-11 produces four isoforms: two from the external promoter and two from the internal promoter. The internal promoter regulates expression of tmy-1 in the pharynx and intestine. By promoter deletion of tmy-1 reporters, a 100 bp fragment was identified that contained binding sequences for a GATA factor, for a chicken CdxA homolog and for a forkhead factor. Both the forkhead and CdxA binding sequences contributed to pharyngeal and intestinal expression. In addition, the GATA site also influenced intestinal expression of tmy-1 reporter. We showed that ELT-2 and PHA-4 proteins interact directly with the GATA and forkhead binding sequences, respectively, in gel mobility shift assays. RNAi knockdown of elt-2 diminished tmy-1::gfp expression in the intestine. In contrast to RNAi knockdown of pha-4, expression of tmy-1::gfp in pha-4;smg-1 mutants was slightly weaker to that of the wild type. Ectopic expression of PHA-4 and ELT-2 by heat shock were sufficient to elicit widespread expression of tmy1::lacZ reporter in embryos. We present models by which ELT-2, PHA-4 and CdxA control expression from the internal promoter oftmy-1 in intestine and pharynx. The essential promoter sequence of the body wall troponin C gene, pat-10/tnc-1 has homology to one of three enhancers of CeMyoD gene, hlh-1. We have isolated three hlh-1 enhancer binding proteins including CeMyoD. Other two are CeTIS11, one of Zn finger protein and a NHR family protein. Interestingly ZYX-1 bound enhancer-binding proteins CeMyoD and CeTIS-11, and also affected muscle gene expressions. ZYX-1 consists N-terminal proline rich and C-terminal three LIM domains. We present a model on how these enhancer-binding proteins control body wall muscle gene expressions and orchestrate appropriate number and correct stage of muscle proteins. These regulation mechanisms will help to understand how terminal differentiated genes are expressed under the control of upstream transcription factors in early stage embryo. "


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