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Gene Review

mec-3  -  Protein MEC-3

Caenorhabditis elegans

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High impact information on mec-3

  • mec-3, a homeobox-containing gene that specifies differentiation of the touch receptor neurons in C. elegans [1].
  • We cloned the mec-3 gene by transposon tagging and showed that a mec-3 mutant can be rescued by germ line transformation using a 5.6 kb genomic DNA fragment [1].
  • In a strain in which transforming mec-3 DNA is present in about 50 copies per haploid genome, additional cells express a mec-3-dependent phenotype [1].
  • The arrangement of cysteine residues in this motif, referred to as LIM (for lin-11 isl-1 mec-3), suggests that this region is a metal-binding domain [2].
  • Two tandem copies of this motif are also present amino-terminal to the homeodomains in the proteins encoded by the genes mec-3, which is required for C. elegans touch neuron differentiation, and isl-1, which encodes a rat insulin I gene enhancer-binding protein [2].

Biological context of mec-3

  • Regulation of anterior cell-specific mec-3 expression during asymmetric cell division in C. elegans [3].
  • In a lin-12 glp-1 double mutant, which is disrupted for many cell interactions in which two cells compete for the same fate, mec-3 expression is unaffected [3].
  • In a lin-5 mutant, in which postembryonic blast cells do not complete cell division and become polyploid, blast cells that would give rise to mec-3-expressing daughters instead express mec-3 themselves [3].
  • The putative coding sequence of mec-3 contains a homeobox, suggesting that the mec-3 protein specifies the expression of touch cell differentiation by binding to DNA and regulating transcription of genes that encode the differentiated features of these cells [1].
  • These results indicate that the mec-3 5' region contains target sequences that mediate a genetic switch between alternative fates expressed by sister cells in a stereotyped cell lineage [4].

Anatomical context of mec-3


Regulatory relationships of mec-3

  • The abnormal touch-neuron-like-cells in sem-4 animals express mec-3; we show that a subset also express egl-5 [6].
  • Repression appears to be controlled by several segments: Mutation of region III, region IV, and parts of region I in a mec-3-lacZ fusion results in beta-galactosidase expression in some non-mec-3-expressing sisters of mec-3-positive cells [4].
  • Our results suggest that the mec-3 promoter is activated in all anterior daughters of unc-86-expressing cells [7].

Other interactions of mec-3

  • A subset, the two PLM cells, also express the Hox gene egl-5, an Abdominal-B homolog, which we find is required for correct mec-3 expression in these cells [6].
  • The Caenorhabditis elegans spalt-like gene sem-4 restricts touch cell fate by repressing the selector Hox gene egl-5 and the effector gene mec-3 [6].
  • Two mutations that suppress the egg-laying defect of unc-86 have no effect on the mec-3 expression defect in an unc-86 mutant [3].
  • A mutation in lin-17 causes production of additional mec-3-expressing cells and can have its effect on the cell division that produces a mec-3-expressing cell [3].
  • The homeobox-containing mec-3 gene of C. elegans is expressed in 10 mechanosensory neurons and is necessary for these cells to acquire their fate [3].


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