Cilia are important for the regulation of a number of signalling pathways, and defects in ciliogenesis are associated with a range of ciliopathies. Early steps in intracellular ciliogenesis involve the attachment of distal appendage vesicles and their fusion to form the ciliary vesicle at the mother centriole, which is known to be mediated by Eps15 homology domain protein 1 (EHD1). However, it is unclear how EHD1 is recruited to the centrosome. In this study, Steve Caplan and colleagues (Xie et al, 2019) identify a role for MICAL-like protein 1 (MICAL-L1), an endosomal interaction partner of EHD1, in early ciliogenesis. They show that depletion of MICAL-L1 impaired ciliogenesis to a similar extent to that of EHD1; returning MICAL-L1 to normal levels in depleted cells resulted in a greater percentage of ciliated cells. Indeed, in the absence of MICAL-L1, EHD1 fails to be recruited to the mother centriole. With regard to the underlying mechanism, the authors demonstrate that MICAL-L1 is initially anchored to the centriole through a direct interaction with the α-tubulin–β-tubulin heterodimers and γ-tubulins; this then results in the recruitment of EHD1, which, in turn, facilitates ciliary vesicle formation and cilia growth. Taken together, this work thus describes the endocytic protein MICAL-L1 as a novel component of the centrosome and an important regulator of ciliogenesis.
A novel role for MICAL-L1 in ciliogenesis
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A novel role for MICAL-L1 in ciliogenesis. J Cell Sci 15 November 2019; 132 (22): e2203. doi:
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