期刊
JOURNAL OF CELL SCIENCE
卷 119, 期 19, 页码 4088-4100出版社
COMPANY OF BIOLOGISTS LTD
DOI: 10.1242/jcs.03187
关键词
C. elegans; cilia; IFT; Rab-like; insulin; IGF signaling
类别
资金
- NHLBI NIH HHS [T32 HL07553-22] Funding Source: Medline
- NIDDK NIH HHS [P30DK056336, P30 DK074038, DK65655, DK62758] Funding Source: Medline
- NIGMS NIH HHS [5 T32 GM008111] Funding Source: Medline
Defects in cilia are associated with diseases and developmental abnormalities. Proper cilia function is required for sonic hedgehog and PDGFR alpha signaling in mammals and for insulin-like growth factor (IGF) signaling in Caenorhabditis elegans. However, the role of cilia in these pathways remains unknown. To begin addressing this issue, we are characterizing putative cilia proteins in C. elegans that are predicted to have regulatory rather than structural functions. In this report, we characterized the novel cilia protein T28F3.6 (IFTA-2, intraflagellar transport associated protein 2), which is homologous to the mammalian Rab-like 5 protein. We found that, unlike the intraflagellar transport (IFT) genes, disruption of ifta-2 does not result in overt cilia assembly abnormalities, nor did it cause chemotaxis or osmotic avoidance defects typical of cilia mutants. Rather, ifta-2 null mutants have an extended lifespan phenotype and are defective in dauer formation. Our analysis indicates that these phenotypes result from defects in the DAF-2 (insulin-IGF-1-like) receptor signaling pathway in ciliated sensory neurons. We conclude that IFTA-2 is not a ciliogenic protein but rather is a regulator of specific cilia signaling activities. Interestingly, a mammalian IFTA-2 homolog is also found in cilia, raising the possibility that its function has been conserved during evolution.
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