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Gene Review:

hop-1 - Protein HOP-1

Caenorhabditis elegans

Lakowski, B. et al., Lakowski, B. et al., Wittenburg, N. et al., Westlund, B. et al.

Lakowski, Roelens, Jacob,

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High impact information on hop-1

Mutations in the Caenorhabditis elegans presenilin genes sel-12 and hop-1 result in a defect in the temperature memory of the animals [1].
As other Spr genes encode proteins homologous to components of the CoREST co-repressor complex that interacts with REST, and the INHAT (inhibitor of acetyltransferase) co-repressor complex, our data suggest that all Spr genes may function through the same mechanism that involves transcriptional repression of the hop-1 locus [2].
Like the mammalian complex, the Drosophila complex is required to regulate neuronal gene expression, whereas the C. elegans homologs regulate the expression of the hop-1 presenilin gene, suggesting an ancient conserved function of CoREST complexes in regulating neuronal gene expression [3].

Biological context of hop-1

Animals bearing both hop-1 and sel-12 deletions displayed new phenotypes not observed in animals bearing either single deletion [4].

References

Presenilin is required for proper morphology and function of neurons in C. elegans. Wittenburg, N., Eimer, S., Lakowski, B., Röhrig, S., Rudolph, C., Baumeister, R. Nature (2000) [Pubmed]
Two suppressors of sel-12 encode C2H2 zinc-finger proteins that regulate presenilin transcription in Caenorhabditis elegans. Lakowski, B., Eimer, S., Göbel, C., Böttcher, A., Wagler, B., Baumeister, R. Development (2003) [Pubmed]
CoREST-Like Complexes Regulate Chromatin Modification and Neuronal Gene Expression. Lakowski, B., Roelens, I., Jacob, S. J. Mol. Neurosci. (2006) [Pubmed]
Reverse genetic analysis of Caenorhabditis elegans presenilins reveals redundant but unequal roles for sel-12 and hop-1 in Notch-pathway signaling. Westlund, B., Parry, D., Clover, R., Basson, M., Johnson, C.D. Proc. Natl. Acad. Sci. U.S.A. (1999) [Pubmed]

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