E-GEOD-5800 - Transcription profiling of skin from interferon regulatory factor 6 (Irf6) knockout mice and wild type mice to study the role for Irf6 in epidermal development
Submitted on 8 September 2006, released on 13 November 2007, last updated on 27 March 2012
Transcription factor paralogs may share a common role (e.g. Hox) in staged or overlapping expression in specific tissues. In other examples, members have distinct roles in a range of embryologic, differentiation or response pathways (e.g. Tbx, Pax). 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 display no embryologic abnormalities. Mice deficient for Irf6 have not been reported, but in humans, mutations in IRF6 cause two Mendelian orofacial clefting syndrome, and genetic variation in IRF6 confers risk for isolated cleft lip and palate. 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 novel role for an IRF family member in epidermal development. Experiment Overall Design: Skin from E17.5 mice was removed and flash frozen for RNA extraction and hybridization on Affymetrix microarrays.
transcription profiling by array, co-expression, individual genetic characteristics
Abnormal skin, limb and craniofacial morphogenesis in mice deficient for interferon regulatory factor 6 (Irf6). Christopher R Ingraham, Akira Kinoshita, Shinji Kondo, Baoli Yang, Samin Sajan, Kurt J Trout, Margaret I Malik, Martine Dunnwald, Stephen L Goudy, Michael Lovett, Jeffrey C Murray, Brian C Schutte. Nat Genet 38(11):1335-40 (2006)