
@article {140648,
	title = {IFT88 maintains sensory function by localising signalling proteins along  cilia.},
	journal = {Life Sci Alliance},
	volume = {7},
	year = {2024},
	month = {2024 May},
	abstract = {<p>Ciliary defects cause several ciliopathies, some of which have late onset, suggesting cilia are actively maintained. Still, we have a poor understanding of the mechanisms underlying their maintenance. Here, we show r IFT88 (IFT88/nompB) continues to move along fully formed sensory cilia. We further identify Inactive, a TRPV channel subunit involved in hearing and negative-gravitaxis behaviour, and a yet uncharacterised Guanylyl Cyclase 2d (Gucy2d/CG34357) as IFT88 cargoes. We also show IFT88 binding to the cyclase{\textasciiacute}s intracellular part, which is evolutionarily conserved and mutated in several degenerative retinal diseases, is important for the ciliary localisation of Gucy2d. Finally, acute knockdown of both IFT88 and Gucy2d in ciliated neurons of adult flies caused defects in the maintenance of cilium function, impairing hearing and negative-gravitaxis behaviour, but did not significantly affect ciliary ultrastructure. We conclude that the sensory ciliary function underlying hearing in the adult fly requires an active maintenance program which involves IFT88 and at least two of its signalling transmembrane cargoes, Gucy2d and Inactive.</p>
},
	keywords = {Animals, Cilia, Drosophila, Drosophila melanogaster, Drosophila Proteins, Hearing},
	issn = {2575-1077},
	doi = {10.26508/lsa.202302289},
	author = {Werner, Sascha and Okenve-Ramos, Pilar and Hehlert, Philip and Zitouni, Sihem and Priya, Pranjali and Mendon{\c c}a, Susana and Sporbert, Anje and Spalthoff, Christian and G{\"o}pfert, Martin C and Jana, Swadhin Chandra and Bettencourt-Dias, M{\'o}nica}
}
@article {91469,
	title = {Plk4 triggers autonomous de novo centriole biogenesis and maturation.},
	journal = {J Cell Biol},
	volume = {220},
	year = {2021},
	month = {2021 May 03},
	abstract = {<p>Centrioles form centrosomes and cilia. In most proliferating cells, centrioles assemble through canonical duplication, which is spatially, temporally, and numerically regulated by the cell cycle and the presence of mature centrioles. However, in certain cell types, centrioles assemble de novo, yet by poorly understood mechanisms. Herein, we established a controlled system to investigate de novo centriole biogenesis, using Drosophila melanogaster egg explants overexpressing Polo-like kinase 4 (Plk4), a trigger for centriole biogenesis. We show that at a high Plk4 concentration, centrioles form de novo, mature, and duplicate, independently of cell cycle progression and of the presence of other centrioles. Plk4 concentration determines the temporal onset of centriole assembly. Moreover, our results suggest that distinct biochemical kinetics regulate de novo and canonical biogenesis. Finally, we investigated which other factors modulate de novo centriole assembly and found that proteins of the pericentriolar material (PCM), and in particular γ-tubulin, promote biogenesis, likely by locally concentrating critical components.</p>
},
	issn = {1540-8140},
	doi = {10.1083/jcb.202008090},
	author = {Nabais, Catarina and Pessoa, Delphine and de-Carvalho, Jorge and van Zanten, Thomas and Duarte, Paulo and Mayor, Satyajit and Carneiro, Jorge and Telley, Ivo A and Bettencourt-Dias, M{\'o}nica}
}
