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- Publisher Website: 10.1083/jcb.201110049
- Scopus: eid_2-s2.0-84864021901
- PMID: 22689656
- WOS: WOS:000305280200010
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Article: The IFT-A complex regulates Shh signaling through cilia structure and membrane protein trafficking
Title | The IFT-A complex regulates Shh signaling through cilia structure and membrane protein trafficking |
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Authors | |
Issue Date | 2012 |
Citation | Journal of Cell Biology, 2012, v. 197, n. 6, p. 789-800 How to Cite? |
Abstract | 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. © 2012 Liem et al. |
Persistent Identifier | http://hdl.handle.net/10722/298569 |
ISSN | 2023 Impact Factor: 7.4 2023 SCImago Journal Rankings: 3.717 |
PubMed Central ID | |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Liem, Karel F. | - |
dc.contributor.author | Ashe, Alyson | - |
dc.contributor.author | He, Mu | - |
dc.contributor.author | Satir, Peter | - |
dc.contributor.author | Moran, Jennifer | - |
dc.contributor.author | Beier, David | - |
dc.contributor.author | Wicking, Carol | - |
dc.contributor.author | Anderson, Kathryn V. | - |
dc.date.accessioned | 2021-04-08T03:08:47Z | - |
dc.date.available | 2021-04-08T03:08:47Z | - |
dc.date.issued | 2012 | - |
dc.identifier.citation | Journal of Cell Biology, 2012, v. 197, n. 6, p. 789-800 | - |
dc.identifier.issn | 0021-9525 | - |
dc.identifier.uri | http://hdl.handle.net/10722/298569 | - |
dc.description.abstract | 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. © 2012 Liem et al. | - |
dc.language | eng | - |
dc.relation.ispartof | Journal of Cell Biology | - |
dc.rights | This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. | - |
dc.title | The IFT-A complex regulates Shh signaling through cilia structure and membrane protein trafficking | - |
dc.type | Article | - |
dc.description.nature | published_or_final_version | - |
dc.identifier.doi | 10.1083/jcb.201110049 | - |
dc.identifier.pmid | 22689656 | - |
dc.identifier.pmcid | PMC3373400 | - |
dc.identifier.scopus | eid_2-s2.0-84864021901 | - |
dc.identifier.volume | 197 | - |
dc.identifier.issue | 6 | - |
dc.identifier.spage | 789 | - |
dc.identifier.epage | 800 | - |
dc.identifier.eissn | 1540-8140 | - |
dc.identifier.isi | WOS:000305280200010 | - |
dc.identifier.issnl | 0021-9525 | - |