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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Gene Review: 

slo-1  -  Protein SLO-1

Caenorhabditis elegans

 
 
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High impact information on slo-1

  • Numerous loss-of-function slo-1 alleles emerged from our screens, indicating that slo-1 has a central role in ethanol responses. slo-1 encodes the BK potassium channel [1].
  • Inactivation of the slo-1 gene in muscles leads to phenotypes similar to those caused by mutations of the dystrophin homologue dys-1 [2].
  • Notably, slo-1 mutations result in a progressive muscle degeneration when put into a sensitized genetic background. slo-1 localization was observed by gfp reporter gene in both the M-line and the dense bodies (Z line) of the C.elegans body-wall muscles [2].
  • The slo-1 and egl-30 mutations conferred resistance to VAs, but unc-43 mutations did not [3].
  • Two putative homologues of large conductance Ca(2+)-activated K(+) channel alpha-subunit gene (slowpoke or slo) were revealed by C. elegans genome sequencing [4].
 

Associations of slo-1 with chemical compounds

  • Moreover, behaviors of slo-1 gain-of-function mutants resemble those of ethanol-intoxicated animals [1].

References

  1. A central role of the BK potassium channel in behavioral responses to ethanol in C. elegans. Davies, A.G., Pierce-Shimomura, J.T., Kim, H., VanHoven, M.K., Thiele, T.R., Bonci, A., Bargmann, C.I., McIntire, S.L. Cell (2003) [Pubmed]
  2. The SLO-1 BK channel of Caenorhabditis elegans is critical for muscle function and is involved in dystrophin-dependent muscle dystrophy. Carre-Pierrat, M., Grisoni, K., Gieseler, K., Mariol, M.C., Martin, E., Jospin, M., Allard, B., Ségalat, L. J. Mol. Biol. (2006) [Pubmed]
  3. Resistance to volatile anesthetics by mutations enhancing excitatory neurotransmitter release in Caenorhabditis elegans. Hawasli, A.H., Saifee, O., Liu, C., Nonet, M.L., Crowder, C.M. Genetics (2004) [Pubmed]
  4. Identification and characterization of a putative C. elegans potassium channel gene (Ce-slo-2) distantly related to Ca(2+)-activated K(+) channels. Lim, H.H., Park, B.J., Choi, H.S., Park, C.S., Eom, S.H., Ahnn, J. Gene (1999) [Pubmed]
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