Journal
NATURE GENETICS
Volume 38, Issue 11, Pages 1335-1340Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ng1903
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Funding
- NIDCR NIH HHS [DE08559, P50 DE016215-01, DE16215, R37 DE008559, R01 DE013513, R01 DE008559-10, R01 DE008559, P50 DE016215, DE13513] Funding Source: Medline
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Transcription factor paralogs may share a common role in staged or overlapping expression in specific tissues, as in the Hox family. In other cases, family members have distinct roles in a range of embryologic, differentiation or response pathways (as in the Tbx and Pax families). For the interferon regulatory factor (IRF) family of transcription factors, mice deficient in Irf1, Irf2, Irf3, Irf4, Irf5, Irf7, Irf8 or Irf9 have defects in the immune response but show no embryologic abnormalities(1-7). Mice deficient for Irf6 have not been reported, but in humans, mutations in IRF6 cause two mendelian orofacial clefting syndromes(8-10), and genetic variation in IRF6 confers risk for isolated cleft lip and palate(11-15). Here we report that mice deficient for Irf6 have abnormal skin, limb and craniofacial development. Histological and gene expression analyses indicate that the primary defect is in keratinocyte differentiation and proliferation. This study describes a new role for an IRF family member in epidermal development.
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