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Gene Review

tax-2  -  Protein TAX-2

Caenorhabditis elegans

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Psychiatry related information on tax-2


High impact information on tax-2

  • We show that mutations in tax-2 or tax-4 disrupt social feeding, and that tax-4 is required in several neurons for social feeding, including one or more of AQR, PQR and URX [2].
  • Some sensory neurons display axon outgrowth defects in tax-2 mutants [1].
  • TAX-2 and TAX-4 have been proposed to form a transduction channel for chemosensation and thermosensation, and tax-2 activity is required in the adult stage for normal chemotaxis to NaCl and odorants [3].

Biological context of tax-2

  • Several classes of mutants (dyf, daf-3, tax-4, and tax-2) that are defective in dauer formation at lower temperatures reverse their phenotypes at 27 degrees and form dauers constitutively [4].

Anatomical context of tax-2

  • The tax-2 and tax-4 genes of C. elegans encode two subunits of a cyclic nucleotide-gated channel that is required for chemosensation, thermosensation and normal axon outgrowth of some sensory neurons [3].

Associations of tax-2 with chemical compounds

  • NPR-1 activity in AQR, PQR and URX neurons seems to suppress social feeding by antagonizing signalling through a cyclic GMP-gated ion channel encoded by tax-2 and tax-4 [2].

Other interactions of tax-2

  • Here we show that, in tax-2 and tax-4 mutants, young larvae have superficially normal axons, but axon outgrowth resumes in inappropriate regions in late larval stages [3].


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