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Gene Review: 

hda-1  -  Protein HDA-1

Caenorhabditis elegans

Synonyms: C53A5.3, Histone deacetylase 1
 
 
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Disease relevance of hda-1

  • Previous studies showed that a mutation in hda-1, e1795, or reduction of hda-1 RNA by RNAi causes defective vulval and gonadal development leading to sterility [1].
 

High impact information on hda-1

  • Our results identify KIN-29 as a new regulator of MEF2/HDAC functions in the nervous system, reveal cell-specific mechanisms of action of this pathway in vivo and demonstrate remarkable complexity in the regulation of CR gene expression in C. elegans [2].
  • In Caenorhabditis elegans, histone acetyltransferase CBP-1 counteracts the repressive activity of the histone deacetylase HDA-1 to allow endoderm differentiation, which is specified by the E cell [3].
  • Here, we show that components of the nucleosome remodelling and histone deacetylase (NURD) complex [1] [2] [3] [4] [5] antagonise vulval development, which is induced by the Ras signal transduction pathway [4].
  • Unlike the previously reported hda-1 mutation, hda-1(cw2) mutants are viable as homozygotes, although many die as embryos or larvae, and are severely uncoordinated [1].
  • The C. elegans histone deacetylase HDA-1 is required for cell migration and axon pathfinding [1].

References

  1. The C. elegans histone deacetylase HDA-1 is required for cell migration and axon pathfinding. Zinovyeva, A.Y., Graham, S.M., Cloud, V.J., Forrester, W.C. Dev. Biol. (2006) [Pubmed]
  2. KIN-29 SIK regulates chemoreceptor gene expression via an MEF2 transcription factor and a class II HDAC. van der Linden, A.M., Nolan, K.M., Sengupta, P. EMBO J. (2007) [Pubmed]
  3. A POP-1 repressor complex restricts inappropriate cell type-specific gene transcription during Caenorhabditis elegans embryogenesis. Calvo, D., Victor, M., Gay, F., Sui, G., Luke, M.P., Dufourcq, P., Wen, G., Maduro, M., Rothman, J., Shi, Y. EMBO J. (2001) [Pubmed]
  4. NURD-complex genes antagonise Ras-induced vulval development in Caenorhabditis elegans. Solari, F., Ahringer, J. Curr. Biol. (2000) [Pubmed]
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