Abstract
Primary cilia rely on compartmentalisation mechanisms that establish the organelle's protein and lipid composition. In mammalian cells, septin GTPases are reported to facilitate cilium formation, function and molecular composition by regulating a membrane diffusion barrier at the ciliary base transition zone (TZ). Here, we examined septins in vivo, within Caenorhabditis elegans sense organs. Unexpectedly, loss of one or both septin genes (unc-59, unc-61) does not cause global defects in cilium structure. Instead, only a subset of ciliated neurons, including the phasmid tail neurons, are affected, with septin mutants displaying short and mispositioned ciliary axonemes due to truncated dendritic processes. Notably, nematode septins do not appear to function at the TZs, with mutants retaining normal gating function and gating complex (MKS & NPHP modules) localisations. Furthermore, double mutant analyses reveal a lack of septin gene interaction with the gating pathways. Strikingly, cell-specific rescue experiments show that UNC-61 regulates phasmid neuronal cilia via a cell non-autonomous mechanism, within supporting glial cells. In addition, UNC-61 localises close to sensory pore adherens cell junctions, and we provide evidence that septin loss disrupts their integrity. Together, our data uncovers an unexpected cell non-autonomous function for glial septins in regulating a subset of sensory neuronal cilia, via a mechanism that may involve cell-cell junctions.