The Zn Finger protein Iguana impacts Hedgehog signaling by promoting ciliogenesis
Hedgehog signaling is critical for metazoan development and requires cilia for pathway activity. The gene iguana was discovered in zebrafish as required for Hedgehog signaling, and encodes a novel Zn finger protein. Planarians are flatworms with robust regenerative capacities and utilize epidermal c...
| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | en_US |
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Elsevier
2010
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| Online Access: | http://hdl.handle.net/1721.1/53334 https://orcid.org/0000-0002-3829-5612 https://orcid.org/0000-0002-5569-333X |
| _version_ | 1811092692929609728 |
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| author | Glazer, Andrew M. Wilkinson, Alex W. Backer, Chelsea B. Gutzman, Jennifer H. Reddien, Peter Lapan, Sylvain W. Cheeseman, Iain M |
| author2 | Massachusetts Institute of Technology. Department of Biology |
| author_facet | Massachusetts Institute of Technology. Department of Biology Glazer, Andrew M. Wilkinson, Alex W. Backer, Chelsea B. Gutzman, Jennifer H. Reddien, Peter Lapan, Sylvain W. Cheeseman, Iain M |
| author_sort | Glazer, Andrew M. |
| collection | MIT |
| description | Hedgehog signaling is critical for metazoan development and requires cilia for pathway activity. The gene iguana was discovered in zebrafish as required for Hedgehog signaling, and encodes a novel Zn finger protein. Planarians are flatworms with robust regenerative capacities and utilize epidermal cilia for locomotion. RNA interference of Smed-iguana in the planarian Schmidtea mediterranea caused cilia loss and failure to regenerate new cilia, but did not cause defects similar to those observed in hedgehog(RNAi) animals. Smed-iguana gene expression was also similar in pattern to the expression of multiple other ciliogenesis genes, but was not required for expression of these ciliogenesis genes. iguana-defective zebrafish had too few motile cilia in pronephric ducts and in Kupffer's vesicle. Kupffer's vesicle promotes left–right asymmetry and iguana mutant embryos had left–right asymmetry defects. Finally, human Iguana proteins (dZIP1 and dZIP1L) localize to the basal bodies of primary cilia and, together, are required for primary cilia formation. Our results indicate that a critical and broadly conserved function for Iguana is in ciliogenesis and that this function has come to be required for Hedgehog signaling in vertebrates. |
| first_indexed | 2024-09-23T15:22:19Z |
| format | Article |
| id | mit-1721.1/53334 |
| institution | Massachusetts Institute of Technology |
| language | en_US |
| last_indexed | 2024-09-23T15:22:19Z |
| publishDate | 2010 |
| publisher | Elsevier |
| record_format | dspace |
| spelling | mit-1721.1/533342022-10-02T02:30:41Z The Zn Finger protein Iguana impacts Hedgehog signaling by promoting ciliogenesis Glazer, Andrew M. Wilkinson, Alex W. Backer, Chelsea B. Gutzman, Jennifer H. Reddien, Peter Lapan, Sylvain W. Cheeseman, Iain M Massachusetts Institute of Technology. Department of Biology Reddien, Peter Glazer, Andrew M. Lapan, Sylvain William Cheeseman, Iain McPherson Reddien, Peter Hedgehog signaling is critical for metazoan development and requires cilia for pathway activity. The gene iguana was discovered in zebrafish as required for Hedgehog signaling, and encodes a novel Zn finger protein. Planarians are flatworms with robust regenerative capacities and utilize epidermal cilia for locomotion. RNA interference of Smed-iguana in the planarian Schmidtea mediterranea caused cilia loss and failure to regenerate new cilia, but did not cause defects similar to those observed in hedgehog(RNAi) animals. Smed-iguana gene expression was also similar in pattern to the expression of multiple other ciliogenesis genes, but was not required for expression of these ciliogenesis genes. iguana-defective zebrafish had too few motile cilia in pronephric ducts and in Kupffer's vesicle. Kupffer's vesicle promotes left–right asymmetry and iguana mutant embryos had left–right asymmetry defects. Finally, human Iguana proteins (dZIP1 and dZIP1L) localize to the basal bodies of primary cilia and, together, are required for primary cilia formation. Our results indicate that a critical and broadly conserved function for Iguana is in ciliogenesis and that this function has come to be required for Hedgehog signaling in vertebrates. Massachusetts Life Sciences Center Howard Hughes Medical Institute W. M. Keck Foundation Rita Allen Foundation Thomas D. and Virginia W. Cabot Career Development Professorship Smith Foundation Searle Foundation 2010-03-31T19:46:18Z 2010-03-31T19:46:18Z 2009-10 2009-10 Article http://purl.org/eprint/type/SubmittedJournalArticle 0012-1606 1095-564X http://hdl.handle.net/1721.1/53334 Glazer, Andrew M. et al. “The Zn Finger Protein Iguana Impacts Hedgehog Signaling by Promoting Ciliogenesis.” Developmental Biology 337.1 (2010): 148–156. https://orcid.org/0000-0002-3829-5612 https://orcid.org/0000-0002-5569-333X en_US http://dx.doi.org/doi:10.1016/j.ydbio.2009.10.025 Developmental Biology Article is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use. application/pdf Elsevier Elaine Fulton |
| spellingShingle | Glazer, Andrew M. Wilkinson, Alex W. Backer, Chelsea B. Gutzman, Jennifer H. Reddien, Peter Lapan, Sylvain W. Cheeseman, Iain M The Zn Finger protein Iguana impacts Hedgehog signaling by promoting ciliogenesis |
| title | The Zn Finger protein Iguana impacts Hedgehog signaling by promoting ciliogenesis |
| title_full | The Zn Finger protein Iguana impacts Hedgehog signaling by promoting ciliogenesis |
| title_fullStr | The Zn Finger protein Iguana impacts Hedgehog signaling by promoting ciliogenesis |
| title_full_unstemmed | The Zn Finger protein Iguana impacts Hedgehog signaling by promoting ciliogenesis |
| title_short | The Zn Finger protein Iguana impacts Hedgehog signaling by promoting ciliogenesis |
| title_sort | zn finger protein iguana impacts hedgehog signaling by promoting ciliogenesis |
| url | http://hdl.handle.net/1721.1/53334 https://orcid.org/0000-0002-3829-5612 https://orcid.org/0000-0002-5569-333X |
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