Publication: acn-1, a C. elegans homologue of ACE, genetically interacts with the let-7 microRNA and other heterochronic genes
Issued Date
2017-10-02
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15514005
15384101
15384101
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2-s2.0-85029719404
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Mahidol University
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SCOPUS
Bibliographic Citation
Cell Cycle. Vol.16, No.19 (2017), 1800-1809
Suggested Citation
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. Cell Cycle. Vol.16, No.19 (2017), 1800-1809. doi:10.1080/15384101.2017.1344798 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/41774
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Title
acn-1, a C. elegans homologue of ACE, genetically interacts with the let-7 microRNA and other heterochronic genes
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Abstract
© 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.