| First Author | Liem KF Jr | Year | 2012 |
| Journal | J Cell Biol | Volume | 197 |
| Issue | 6 | Pages | 789-800 |
| PubMed ID | 22689656 | Mgi Jnum | J:185270 |
| Mgi Id | MGI:5428054 | Doi | 10.1083/jcb.201110049 |
| Citation | Liem KF Jr, et al. (2012) The IFT-A complex regulates Shh signaling through cilia structure and membrane protein trafficking. J Cell Biol 197(6):789-800 |
| abstractText | Two intraflagellar transport (IFT) complexes, IFT-A and IFT-B, build and maintain primary cilia and are required for activity of the Sonic hedgehog (Shh) pathway. A weak allele of the IFT-A gene, Ift144, caused subtle defects in cilia structure and ectopic activation of the Shh pathway. In contrast, strong loss of IFT-A, caused by either absence of Ift144 or mutations in two IFT-A genes, blocked normal ciliogenesis and decreased Shh signaling. In strong IFT-A mutants, the Shh pathway proteins Gli2, Sufu, and Kif7 localized correctly to cilia tips, suggesting that these pathway components were trafficked by IFT-B. In contrast, the membrane proteins Arl13b, ACIII, and Smo failed to localize to primary cilia in the absence of IFT-A. We propose that the increased Shh activity seen in partial loss-of-function IFT-A mutants may be a result of decreased ciliary ACIII and that the loss of Shh activity in the absence of IFT-A is a result of severe disruptions of cilia structure and membrane protein trafficking. |
