Turan, Merve GulKantarci, HanifeCevik, SebihaKaplan, Oktay I.2025-03-102025-03-1020252589-0042https://doi.org/10.1016/j.isci.2025.111791https://hdl.handle.net/20.500.12573/2441We thank Ferhan Yenisert for her assistance in creating a transgenic strain and Bradley K. Yoder for supplying the plasmid (F16F9.3promoter::GFP, PCP41). Several strains were acquired from the CGC, which is supported by the NIH Office of Research Infrastructure Programs (P40 OD010440), United States. This research was supported by the Health Institutes of Turkey (TUSEB) (Project number: 28555), Turkiye to S.C.The interaction of cilia with various cellular compartments, such as axons, has emerged as a new form of cellular communication. Cilia often extend in proximity to cilia from neighboring cells. However, the mechanisms driving this process termed juxtaposed cilia-cilia elongation (JCE) remain unclear. We use fluorescence-based visualization to study the mechanisms of coordinated cilia elongation in sensory neurons of Caenorhabditis elegans. Conducting a selective gene-based screening strategy reveals that ARL-13/ARL13B and MKS-5/RPGRIP1L are essential for JCE. We demonstrate that ARL-13 modulates JCE independently of cilia length. Loss of NPHP-2/inversin along with HDAC-6 enhances the cilia misdirection phenotype of arl-13 mutants, while disruption of the BBSome complex, but not microtubule components, partially suppresses the JCE defects in arl-13 mutants. We further show changes in the phospholipid compositions in arl-13 mutants. We suggest that ARL-13 contributes to JCE, in part, through the modulation of the ciliary membrane.enginfo:eu-repo/semantics/openAccessFUNCTIONAL REDUNDANCYTUBULIN TRANSPORTJOUBERT SYNDROMESENSORY CILIADISEASE GENESPROTEINCILIOGENESISMUTATIONSFLAGELLARBIOGENESISarticle282119