The balance between proliferation and differentiation is a fundamental aspect of multicellular life. Perhaps nowhere is this delicate balance more palpable than in the multiciliated cells (MCCs) that line the respiratory tract, the ependyma, and the oviduct. These cells contain dozens to hundreds of motile cilia that beat in a concerted fashion to generate directed fluid flow over the tissue surface. Although MCCs have exited the cell cycle, remarkably, they retain the ability to duplicate their centrioles and to mature those centrioles into ciliary basal bodies—two features, which are known to be normally under strict cell cycle control (Firat‐Karalar & Stearns, 2014). How post‐mitotic MCCs retain this ability, remains unclear. In the past several months, four research articles, including one from Terré et al in this issue of The EMBO Journal, have described a vital role for the geminin coiled‐coil domain‐containing protein (Gemc1) in the MCC gene expression program in multiple tissues and organisms, that bring us closer to understanding this question (Kyrousi et al, 2015; Zhou et al, 2015; Arbi et al, 2016; Terré et al, 2016).
See also: B Terré et al
and M Arbi et al (March 2016)
Over the past 10 years, multiple MCC differentiation factors have been identified (Brooks & Wallingford, 2014), most of which are transcriptional regulators that act together to launch a massive, MCC‐specific gene expression program that turns on hundreds of regulatory and structural ciliary genes. Interestingly, some of these transcription factors, including c‐Myb, and E2F4 and E2F5 (E2F4/5), also control cell cycle events in other cells. Gemc1 (also known as Gmnc) is a member of the geminin family of nuclear proteins and has a previously defined role in cell cycle‐regulated DNA replication (Balestrini et al, 2010). Data show that Gemc1 is essential for MCC differentiation, and acts together with the other …
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