Disruption of Rab8a and Rab11a causes formation of basolateral microvilli in neonatal enteropathy

Qiang Feng, Edward M. Bonder, Amy C. Engevik, Lanjing Zhang, Matthew J. Tyska, James R. Goldenring, Nan Gao

Research output: Contribution to journalArticlepeer-review

15 Scopus citations


Misplaced formation of microvilli to basolateral domains and intracellular inclusions in enterocytes are pathognomonic features in congenital enteropathy associated with mutation of the apical plasma membrane receptor syntaxin 3 (STX3). Although the demonstrated binding of Myo5b to the Rab8a and Rab11a small GTPases in vitro implicates cytoskeleton-dependent membrane sorting, the mechanisms underlying the microvillar location defect remain unclear. By selective or combinatory disruption of Rab8a and Rab11a membrane traffic in vivo, we demonstrate that transport of distinct cargo to the apical brush border rely on either individual or both Rab regulators, whereas certain basolateral cargos are redundantly transported by both factors. Enterocyte-specific Rab8a and Rab11a double-knockout mouse neonates showed immediate postnatal lethality and more severe enteropathy than single knockouts, with extensive formation of microvilli along basolateral surfaces. Notably, following an inducible Rab11a deletion from neonatal enterocytes, basolateral microvilli were induced within 3 days. These data identify a potentially important and distinct mechanism for a characteristic microvillus defect exhibited by enterocytes of patients with neonatal enteropathy.

Original languageAmerican English
Pages (from-to)2491-2505
Number of pages15
JournalJournal of cell science
Issue number15
StatePublished - Aug 1 2017

ASJC Scopus subject areas

  • Cell Biology


  • Enterocyte
  • Microvillus formation
  • Neonatal enteropathy
  • Rab11a
  • Rab8a


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