GSE123017
Differential requirement for centriolar satellites in cilium formation and ciliary signaling among different vertebrate cells
Centriolar satellites are an array of membrane-less granules that localize and  move around the vertebrate centrosome/cilium complex. They have recently  emerged as key regulators of the biogenesis and function of the  centrosome/cilium-complex and their mutations are linked to ciliopathies.  Although centriolar satellites are ubiquitous structures of the vertebrate cells,  their precise function and molecular mechanism of action in different cell types  remain poorly understood. Here, we generated kidney and retinal epithelial cells  that lack centriolar satellites by genetically ablating their scaffolding protein  PCM1 and investigated the cellular and molecular consequences of satellite loss  in cells. We showed that centriolar satellites are required for cilium assembly,  regulation of ciliary content, timely response to Hedgehog signals and three-  dimensional epithelial cell organization, but not for cell proliferation, cell cycle  progression and centriole duplication. Importantly, the requirement for centriolar  satellites in cilium assembly varied between retinal and kidney epithelial cells and  we identified the differences in the efficiency of targeting key ciliogenesis factors  to the centrosome including Mib1 and Talpid3 as the likely molecular basis for  this phenotypic variability. Quantitative global transcriptomic and proteomic  profiling of satellite-less cells showed that loss of centriolar satellites does not  lead to a major transcriptional response, but leads to a significant rearrangement  of the global proteome. Together, our findings identify important roles for  centriolar satellites in key cilium-related cellular processes through regulating the  proteostasis and centrosomal/ciliary targeting of proteins and provide insight into  the disease mechanisms of ciliopathies. Overall design: We performed global transcriptome analysis of wild type (WT) and PCM1 knock-out cells by using two different cells: human RPE1, and mouse IMCD3 cells. Deep sequencing technique was utilized via  illumina HiSeq4000 platfrom in two biological replicates for each condition.