Cystic canal mutants in Caenorhabditis elegans are defective in the apical membrane domain of the renal (excretory) cell

Matthew Buechner, David H. Hall, Harshida Bhatt, Edward M. Hedgecock

Research output: Contribution to journalArticlepeer-review

108 Scopus citations

Abstract

The excretory cell extends a tubular process, or canal, along the basolateral surface of the epidermis to form the nematode renal epithelium. This cell can undergo normal tubulogenesis in isolated cell culture. Mutations in 12 genes cause excretory canal cysts in Caenorhabditis elegans. Genetic interactions, and their similar phenotypes, suggest these genes may encode functionally related proteins. Depending upon genotype and individual canal, defects range from focal cysts, flanked by normal width segments, to regional cysts involving the entire tubule. Oftentimes the enlarged regions are convoluted or partially septated. In mutants with very large cysts, renal function is measurably impaired. Based on histology and ultrastructure, canal cysts likely result from defects of the apical membrane domain. These mutants provide a model of tubulocystic disease without hyperplasia or basement membrane abnormalities. Similar apical mechanisms could regulate tubular morphology of vertebrate nephrons.

Original languageEnglish (US)
Pages (from-to)227-241
Number of pages15
JournalDevelopmental Biology
Volume214
Issue number1
DOIs
StatePublished - Oct 1 1999

Keywords

  • Excretory canals
  • Nematode
  • Polycystic kidney disease
  • Renal epithelium
  • Tubulogenesis

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology
  • Cell Biology

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