Epidermal cells are renewed by the proliferative capacity of progenitor cells in the basal layer. The progenitor cells either divide asymmetrically or delaminate in order to contribute to the differentiated stratified layers. Such balance between differentiation and proliferation is controlled through several mechanisms. Moreover, epidermal differentiation has been associated with a block in mitosis and an increase in the ploidy, but the underlying mechanisms are unknown. In this issue (p. 683), Mirna Perez-Moreno and co-workers investigate the role of the microtubule plus-end-binding protein Clasp2, which localises to the plus-end of microtubules at cell adhesion sites in the basal progenitor layer of the epidermis. The authors show that loss of Clasp2 expression in mouse and human basal keratinocytes results in premature differentiation, as increased gene expression of differentiation markers is observed upon Clasp2 downregulation. Further, these cells display a high DNA content and increased polyploidy. Loss of Clasp2 also leads to an increase in centrosome numbers in interphase and disorganised mitotic spindles. The authors also demonstrate that premature differentiation of keratinocytes in absence of Clasp2 is also associated with DNA damage and p53 activation. Together, these data show that Clasp2 is required for mitotic fidelity and to keep primary keratinocytes in an undifferentiated state.
- © 2017. Published by The Company of Biologists Ltd