| Role of epidermal primary cilia in the homeostasis of skin and hair follicles. | |
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MedLine Citation:
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PMID: 21429982 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Skin and hair follicle morphogenesis and homeostasis require the integration of multiple signaling pathways, including Hedgehog (Hh) and Wingless (Wnt), and oriented cell divisions, all of which have been associated with primary cilia. Although studies have shown that disrupting dermal cilia causes follicular arrest and attenuated Hh signaling, little is known about the role of epidermal cilia. Here, epidermal cilia function was analyzed using conditional alleles of the ciliogenic genes Ift88 and Kif3a. At birth, epidermal cilia mutants appeared normal, but developed basaloid hyperplasia and ingrowths into the dermis of the ventrum with age. In addition, follicles in the tail were disorganized and had excess sebaceous gland lobules. Epidermal cilia mutants displayed fewer long-term label-retaining cells, suggesting altered stem cell homeostasis. Abnormal proliferation and differentiation were evident from lineage-tracing studies and showed an expansion of follicular cells into the interfollicular epidermis, as is seen during wound repair. These phenotypes were not associated with changes in canonical Wnt activity or oriented cell division. However, nuclear accumulation of the ΔNp63 transcription factor, which is involved in stratification, keratinocyte differentiation and wound repair, was increased, whereas the Hh pathway was repressed. Intriguingly, the phenotypes were not typical of those associated with loss of Hh signaling but exhibited similarities with those of mice in which ΔNp63 is overexpressed in the epidermis. Collectively, these data indicate that epidermal primary cilia may function in stress responses and epidermal homeostasis involving pathways other than those typically associated with primary cilia. |
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Authors:
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Mandy J Croyle; Jonathan M Lehman; Amber K O'Connor; Sunny Y Wong; Erik B Malarkey; Daniela Iribarne; William E Dowdle; Trenton R Schoeb; Zoe M Verney; Mohammad Athar; Edward J Michaud; Jeremy F Reiter; Bradley K Yoder |
Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2011-03-23 |
Journal Detail:
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Title: Development (Cambridge, England) Volume: 138 ISSN: 1477-9129 ISO Abbreviation: Development Publication Date: 2011 May |
Date Detail:
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Created Date: 2011-04-13 Completed Date: 2011-07-01 Revised Date: 2012-09-20 |
Medline Journal Info:
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Nlm Unique ID: 8701744 Medline TA: Development Country: England |
Other Details:
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Languages: eng Pagination: 1675-85 Citation Subset: IM |
Affiliation:
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Department of Cell Biology, University of Alabama at Birmingham Medical School, Birmingham, AL 35294, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Animals, Newborn Cilia / genetics, metabolism, physiology* Epidermis / cytology*, metabolism, physiology Gene Expression Regulation, Developmental Hair Follicle / cytology, metabolism, physiology* Homeostasis / genetics, physiology* Integrases / genetics, metabolism Kinesin / genetics, metabolism Mice Mice, Inbred C57BL Mice, Transgenic Phenotype Skin Physiological Processes* / genetics Transgenes / genetics Tumor Suppressor Proteins / genetics, metabolism |
| Grant Support | |
ID/Acronym/Agency:
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1K99AR059796/AR/NIAMS NIH HHS; AR054396/AR/NIAMS NIH HHS; ES015323/ES/NIEHS NIH HHS; R01 AR052792/AR/NIAMS NIH HHS; R01 HD056030/HD/NICHD NIH HHS; T32 AR047512-07/AR/NIAMS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Kif3a protein, mouse; 0/Tg737Rpw protein, mouse; 0/Tumor Suppressor Proteins; EC 2.7.7.-/Cre recombinase; EC 2.7.7.-/Integrases; EC 3.6.1.-/Kinesin |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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