acn-1, a C. elegans homologue of ACE, genetically interacts with the let-7 microRNA and other heterochronic genes
© 2017 Taylor & Francis. The heterochronic pathway in C. elegans controls the relative timing of cell fate decisions during post-embryonic development. It includes a network of microRNAs (miRNAs), such as let-7, and protein-coding genes, such as the stemness factors, LIN-28 and LIN-41. Here we...
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th-mahidol.417742019-03-14T15:02:46Z acn-1, a C. elegans homologue of ACE, genetically interacts with the let-7 microRNA and other heterochronic genes Chanatip Metheetrairut Yuri Ahuja Frank J. Slack Yale University Mahidol University Harvard Medical School Biochemistry, Genetics and Molecular Biology © 2017 Taylor & Francis. The heterochronic pathway in C. elegans controls the relative timing of cell fate decisions during post-embryonic development. It includes a network of microRNAs (miRNAs), such as let-7, and protein-coding genes, such as the stemness factors, LIN-28 and LIN-41. Here we identified the acn-1 gene, a homologue of mammalian angiotensin-converting enzyme (ACE), as a new suppressor of the stem cell developmental defects of let-7 mutants. Since acn-1 null mutants die during early larval development, we used RNAi to characterize the role of acn-1 in C. elegans seam cell development, and determined its interaction with heterochronic factors, including let-7 and its downstream interactors–lin-41, hbl-1, and apl-1. We demonstrate that although RNAi knockdown of acn-1 is insufficient to cause heterochronic defects on its own, loss of acn-1 suppresses the retarded phenotypes of let-7 mutants and enhances the precocious phenotypes of hbl-1, though not lin-41, mutants. Conversely, the pattern of acn-1 expression, which oscillates during larval development, is disrupted by lin-41 mutants but not by hbl-1 mutants. Finally, we show that acn-1(RNAi) enhances the let-7-suppressing phenotypes caused by loss of apl-1, a homologue of the Alzheimer's disease-causing amyloid precursor protein (APP), while significantly disrupting the expression of apl-1 during the L4 larval stage. In conclusion, acn-1 interacts with heterochronic genes and appears to function downstream of let-7 and its target genes, including lin-41 and apl-1. 2018-12-21T06:40:47Z 2019-03-14T08:02:46Z 2018-12-21T06:40:47Z 2019-03-14T08:02:46Z 2017-10-02 Article Cell Cycle. Vol.16, No.19 (2017), 1800-1809 10.1080/15384101.2017.1344798 15514005 15384101 2-s2.0-85029719404 https://repository.li.mahidol.ac.th/handle/123456789/41774 Mahidol University SCOPUS https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85029719404&origin=inward |
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Biochemistry, Genetics and Molecular Biology Chanatip Metheetrairut Yuri Ahuja Frank J. Slack acn-1, a C. elegans homologue of ACE, genetically interacts with the let-7 microRNA and other heterochronic genes |
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© 2017 Taylor & Francis. The heterochronic pathway in C. elegans controls the relative timing of cell fate decisions during post-embryonic development. It includes a network of microRNAs (miRNAs), such as let-7, and protein-coding genes, such as the stemness factors, LIN-28 and LIN-41. Here we identified the acn-1 gene, a homologue of mammalian angiotensin-converting enzyme (ACE), as a new suppressor of the stem cell developmental defects of let-7 mutants. Since acn-1 null mutants die during early larval development, we used RNAi to characterize the role of acn-1 in C. elegans seam cell development, and determined its interaction with heterochronic factors, including let-7 and its downstream interactors–lin-41, hbl-1, and apl-1. We demonstrate that although RNAi knockdown of acn-1 is insufficient to cause heterochronic defects on its own, loss of acn-1 suppresses the retarded phenotypes of let-7 mutants and enhances the precocious phenotypes of hbl-1, though not lin-41, mutants. Conversely, the pattern of acn-1 expression, which oscillates during larval development, is disrupted by lin-41 mutants but not by hbl-1 mutants. Finally, we show that acn-1(RNAi) enhances the let-7-suppressing phenotypes caused by loss of apl-1, a homologue of the Alzheimer's disease-causing amyloid precursor protein (APP), while significantly disrupting the expression of apl-1 during the L4 larval stage. In conclusion, acn-1 interacts with heterochronic genes and appears to function downstream of let-7 and its target genes, including lin-41 and apl-1. |
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Yale University |
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Yale University Chanatip Metheetrairut Yuri Ahuja Frank J. Slack |
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Article |
author |
Chanatip Metheetrairut Yuri Ahuja Frank J. Slack |
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Chanatip Metheetrairut |
title |
acn-1, a C. elegans homologue of ACE, genetically interacts with the let-7 microRNA and other heterochronic genes |
title_short |
acn-1, a C. elegans homologue of ACE, genetically interacts with the let-7 microRNA and other heterochronic genes |
title_full |
acn-1, a C. elegans homologue of ACE, genetically interacts with the let-7 microRNA and other heterochronic genes |
title_fullStr |
acn-1, a C. elegans homologue of ACE, genetically interacts with the let-7 microRNA and other heterochronic genes |
title_full_unstemmed |
acn-1, a C. elegans homologue of ACE, genetically interacts with the let-7 microRNA and other heterochronic genes |
title_sort |
acn-1, a c. elegans homologue of ace, genetically interacts with the let-7 microrna and other heterochronic genes |
publishDate |
2018 |
url |
https://repository.li.mahidol.ac.th/handle/123456789/41774 |
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1763494743555178496 |