Keratin 17 modulates hair follicle cycling in a TNFα-dependent fashion

Xuemei Tong, Pierre A. Coulombe

Research output: Contribution to journalArticlepeer-review


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 TNFα. 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 TNFα signaling. The activity of NF-θB, a downstream target of TNFα, is increased in K17-null skin. We also find that TNFα 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 TNFα as two novel and interdependent regulators of hair cycling.

Original languageEnglish (US)
Pages (from-to)1353-1364
Number of pages12
JournalGenes and Development
Issue number10
StatePublished - May 15 2006
Externally publishedYes


  • Anagen
  • Apoptosis
  • Catagen
  • Hair cycle
  • Intermediate filament

ASJC Scopus subject areas

  • Genetics
  • Developmental Biology


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