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. 2017 Oct 27;25(1):144–153. doi: 10.1038/cdd.2017.178

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Copyright © 2018 The Author(s)

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Selective absence of p73 in mice results in severe abnormalities of ciliogenesis in the airways. (a) Transmission electron microscopy and (b) scanning electron microscopy of the trachea of p73 knockout (p73KO) and control (WT) mice at 2 months of age. The p73-deficient mice show highly defective, rare, short, stump-like cilia (arrow). Asterix, microvilli. TAp73KO mice have a similar phenotype. (c) Measuring mucociliary transport. Aggregated fluorescent bead trajectories in control (WT) versus TAp73KO tracheae. WT trajectories (red arrow) follow a directional flow field that is completely lost in knockout tracheae. (d) Distribution of particle velocities (measured as μm/s) from WT, TAp73KO and WT diffusion control (formalin-fixed) tracheae as in panel c. (e) Proposed role of TAp73 as master transcriptional regulator of motile multiciliogenesis in airways, directly controlling Fox, Rfx2/3, Myb and miR34, plus a plethora of ciliary structure/motility genes. Mcidas is upstream of TAp73. Modified with permission from Nemajerova et al., 2016. Asterix indicates genes directly regulated by TAp73. n.s. nonsignificant