Hedgehog signalling in the mouse requires intraflagellar transport proteins

Danwei Huangfu, Aimin Liu, Andrew S. Rakeman, Noel S. Murcia, Lee Niswander and Kathryn V. Anderson ()
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Danwei Huangfu: Sloan-Kettering Institute
Aimin Liu: Sloan-Kettering Institute
Andrew S. Rakeman: Sloan-Kettering Institute
Noel S. Murcia: Case Western Reserve University
Lee Niswander: Sloan-Kettering Institute
Kathryn V. Anderson: Sloan-Kettering Institute

Nature, 2003, vol. 426, issue 6962, 83-87

Abstract: Abstract Intraflagellar transport (IFT) proteins were first identified as essential factors for the growth and maintenance of flagella in the single-celled alga Chlamydomonas reinhardtii1. In a screen for embryonic patterning mutations induced by ethylnitrosourea, here we identify two mouse mutants, wimple (wim) and flexo (fxo), that lack ventral neural cell types and show other phenotypes characteristic of defects in Sonic hedgehog signalling. Both mutations disrupt IFT proteins: the wim mutation is an allele of the previously uncharacterized mouse homologue of IFT172; and fxo is a new hypomorphic allele of polaris, the mouse homologue of IFT88. Genetic analysis shows that Wim, Polaris and the IFT motor protein Kif3a are required for Hedgehog signalling at a step downstream of Patched1 (the Hedgehog receptor) and upstream of direct targets of Hedgehog signalling. Our data show that IFT machinery has an essential and vertebrate-specific role in Hedgehog signal transduction.

Date: 2003
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DOI: 10.1038/nature02061

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