Akt2 and SGK3 Are Both Determinants of Postnatal Hair Follicle Development
May 2009
in “
The FASEB Journal
”
Studysummary This study found that Akt2 and SGK3 are crucial for postnatal hair follicle development in mice, as their combined absence led to severe hair growth defects due to disrupted β-catenin-dependent transcriptional processes. Our plain-language summary of this paper — not a Tressless recommendation.
The study investigated the roles of SGK3 and Akt2 in postnatal hair follicle development in mice. SGK3, a serine-threonine kinase, was previously known to be crucial for hair follicle development, with SGK3-deficient mice showing abnormal follicle cycling that improved with age. However, this was not observed in mice lacking Akt1, Akt2, or Akt3. The researchers created Akt2/SGK3 double knockout (DKO) mice and found that these mice exhibited a more severe hair growth defect than SGK3-deficient mice alone, characterized by accelerated catagen and anagen phases, irregular follicle orientation, and increased sebaceous gland expression. This defect was linked to a failure in follicle matrix cell nuclear β-catenin accumulation and proliferation. Both Akt2 and SGK3 were shown to stimulate β-catenin-LEF1-dependent transcription in keratinocytes, suggesting their redundant roles in regulating β-catenin-dependent transcriptional processes essential for hair follicle cell proliferation.
