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PMID:16702408
| Citation |
Tong, X and Coulombe, PA (2006) Keratin 17 modulates hair follicle cycling in a TNFalpha-dependent fashion. Genes Dev. 20:1353-64 |
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| Abstract |
Mammalian hair follicles cycle between stages of rapid growth (anagen) and metabolic quiescence (telogen) throughout life. Transition from anagen to telogen involves an intermediate stage, catagen, consisting of a swift, apoptosis-driven involution of the lower half of the follicle. How catagen is coordinated, and spares the progenitor cells needed for anagen re-entry, is poorly understood. Keratin 17 (K17)-null mice develop alopecia in the first week post-birth, correlating with hair shaft fragility and untimely apoptosis in the hair bulb. Here we show that this abnormal apoptosis reflects premature entry into catagen. Of the proapoptotic challenges tested, K17-null skin keratinocytes in primary culture are selectively more sensitive to TNFalpha. K17 interacts with TNF receptor 1 (TNFR1)-associated death domain protein (TRADD), a death adaptor essential for TNFR1-dependent signal relay, suggesting a functional link between this keratin and TNFalpha signaling. The activity of NF-kappaB, a downstream target of TNFalpha, is increased in K17-null skin. We also find that TNFalpha is required for a timely anagen-catagen transition in mouse pelage follicles, and that its ablation partially rescues the hair cycling defect of K17-null mice. These findings identify K17 and TNFalpha as two novel and interdependent regulators of hair cycling. |
| Links |
PubMed PMC1472909 Online version:10.1101/gad.1387406 |
| Keywords |
Alopecia/genetics; Animals; Apoptosis/genetics; Cell Cycle/genetics; Hair Follicle/cytology; Hair Follicle/growth & development; Hair Follicle/metabolism; Keratinocytes/cytology; Keratinocytes/metabolism; Keratins/genetics; Keratins/metabolism; Mice; Mice, Mutant Strains; NF-kappa B/metabolism; Signal Transduction; TNF Receptor-Associated Death Domain Protein; Tumor Necrosis Factor Receptor-Associated Peptides and Proteins/metabolism; Tumor Necrosis Factor-alpha/genetics; Tumor Necrosis Factor-alpha/metabolism |
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Significance
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| Gene product | Qualifier | GO ID | GO term name | Evidence Code | with/from | Aspect | Notes | Status |
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