Document Detail


Role of epidermal primary cilia in the homeostasis of skin and hair follicles.
MedLine Citation:
PMID:  21429982     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
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:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-03-23
Journal Detail:
Title:  Development (Cambridge, England)     Volume:  138     ISSN:  1477-9129     ISO Abbreviation:  Development     Publication Date:  2011 May 
Date Detail:
Created Date:  2011-04-13     Completed Date:  2011-07-01     Revised Date:  2013-06-30    
Medline Journal Info:
Nlm Unique ID:  8701744     Medline TA:  Development     Country:  England    
Other Details:
Languages:  eng     Pagination:  1675-85     Citation Subset:  IM    
Affiliation:
Department of Cell Biology, University of Alabama at Birmingham Medical School, Birmingham, AL 35294, USA.
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MeSH Terms
Descriptor/Qualifier:
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:
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:
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

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