It is found that these cells rarely divide within their niche but change properties abruptly when stimulated to exit, and their transcriptional profile is determined, which, when compared to progeny and other SCs, defines the niche.
It is demonstrated that LEF1/TCF3 is necessary but not sufficient for TOPGAL activation, revealing the existence of positive and negative regulators of these factors in the skin and unveiling the importance of activated LEF/ TCF complexes at distinct times in hair development and cycling when changes in cell fate and differentiation commitments take place.
A dynamic mechanism for intercellular adhesion is unveiled involving calcium-activated filopodia penetration and VASP/Mena-dependent actin reorganization/polymerization.
It is suggested that the niche microenvironment imposes intrinsic "stemness" features without restricting the establishment of epithelial polarity and changes in gene expression.
It is shown that HG cells are derived from bulge stem cells (SCs) but become responsive quicker to DP-promoting signals, and also proliferate sooner but display shorter-lived potential than bulge cells.
It is shown that basal epidermal cells use their polarity to divide asymmetrically, generating a committed suprabasal cell and a proliferative basal cell and it is demonstrated that integrins and cadherins are essential for the apical localization of atypical protein kinase C, the Par3–LGN–Inscuteable complex and NuMA–dynactin to align the spindle.
This review, which examines adult stem cell niches and their impact on stem cell biology, highlights the importance of understanding how stem cells interact with their microenvironment to establish and maintain their properties.
A modified method of whole-mount in situ hybridization was used to track skin-specific expression of endogenous keratin mRNAs throughout embryogenesis, and it was demonstrated that AP2 has a strong inductive effect on basal keratin expression in a cellular environment that does not normally possess AP2 activity.
It is reported that this pathway operates in keratinocytes and that mice expressing a stabilized beta-catenin controlled by an epidermal promoter undergo a process resembling de novo hair morphogenesis, suggesting that transient beta-Catenin stabilization may be a key player in the long-sought epidersmal signal leading to hair development and implicate aberrant beta- catenin activation in hair tumors.