Understanding the Molecular Mechanisms of Hair Follicle Stem Cell Quiescence and Genome Plasticity

The study explored the molecular mechanisms of hair follicle stem cell quiescence and its relation to fate determination. It revealed that the transcription factor Runx1 regulates Cyclin-Dependent Kinase inhibitors (CDKis) like p15, p21, p27, and p57, which are crucial for maintaining quiescence. The absence of p21 disrupted timely quiescence entry, and Runx1's interaction with p21 was context-dependent. Additionally, CDKis were found to regulate transcription of other CDKis independently of their kinase-inhibitory function. The study also highlighted the role of histone methylation in quiescence, with low levels of H3K4me3, H3K9me3, and H3K27me3 linked to higher genome plasticity, facilitating fate decisions. These findings suggested a robust mechanism for maintaining quiescence, associating it with plasticity for fate determination.