sel-7, a positive regulator of lin-12 activity, encodes a novel nuclear protein in Caenorhabditis elegans

Genetics. 2004 Jan;166(1):151-60. doi: 10.1534/genetics.166.1.151.

Abstract

Suppressor genetics in C. elegans has identified key components of the LIN-12/Notch signaling pathway. Here, we describe a genetic and molecular characterization of the suppressor gene sel-7. We show that reducing or eliminating sel-7 activity suppresses the effects of constitutive lin-12 activity, enhances the effects of partially reduced lin-12 activity, and causes a synthetic Lin-12(0) phenotype when combined with a null mutation in the sel-12 presenilin gene. These observations suggest that sel-7 is a positive regulator of lin-12 activity. We also show that SEL-7 encodes a novel nuclear protein. Through yeast two-hybrid screening, we identified an apparent interaction partner, K08E3.8, that also interacts with SEL-8, a known component of the nuclear complex that forms upon LIN-12 activation. Our data suggest potential roles for SEL-7 in the assembly or function of this nuclear complex.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Base Sequence
  • Caenorhabditis elegans Proteins / genetics*
  • Caenorhabditis elegans Proteins / metabolism*
  • Carrier Proteins / genetics
  • Carrier Proteins / metabolism
  • DNA, Helminth / genetics
  • Genes, Helminth
  • Membrane Proteins / genetics*
  • Membrane Proteins / metabolism*
  • Models, Biological
  • Molecular Sequence Data
  • Mutation
  • Nuclear Proteins / genetics
  • Nuclear Proteins / metabolism
  • Phenotype
  • Receptors, Notch
  • Sequence Homology, Amino Acid
  • Suppression, Genetic
  • Transcription Factors / genetics*
  • Transcription Factors / metabolism*
  • Two-Hybrid System Techniques

Substances

  • Caenorhabditis elegans Proteins
  • Carrier Proteins
  • DNA, Helminth
  • Lin-12 protein, C elegans
  • Membrane Proteins
  • Nuclear Proteins
  • Receptors, Notch
  • Sel-7 protein, C elegans
  • Transcription Factors