Signaling from Keratins

The study by Seyun Kim, Pauline Wong, and Pierre Coulombe revealed that Keratin 17 (K17) played a crucial signaling role in cell growth during wound healing, beyond its structural function. In embryos lacking K17, wound healing was impaired not due to structural issues but because of a block in mTOR-activated protein synthesis. Normally, K17 is activated in wound-adjacent epithelial cells, promoting growth and migration into the wound site. However, in K17 mutants, this process was stunted. The study found that the 14-3-3σ adaptor protein, which contributes to mTOR activation, was associated with cytoplasmic K17 filaments in normal cells but was mostly nuclear in K17-deficient cells. This suggested that K17 might facilitate mTOR pathway components' assembly, although the exact mechanism remained unclear. Additionally, keratins were found to delay apoptosis in hair follicles, indicating their complex regulatory roles beyond mechanical support.