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首页> 外文期刊>Cell cycle >acn-1, a C-elegans homologue of ACE, genetically interacts with the let-7 microRNA and other heterochronic genes
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acn-1, a C-elegans homologue of ACE, genetically interacts with the let-7 microRNA and other heterochronic genes

机译：ACN-1，ACE的C-elegans同源物，遗传与Let-7 microRNA和其他异化基因相互作用

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摘要

The heterochronic pathway in C. elegans controls the relative timing of cell fate decisions during postembryonic 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.
机译：C.Cegris的异形途径控制后术后细胞命运决策的相对时间。它包括微大RNA（miRNA）的网络，例如Let-7和蛋白质编码基因，例如茎秆因子，LIN-28和LIN-41。在这里，我们鉴定了哺乳动物血管紧张素转换酶（ACE）的同源物的ACN-1基因，作为Let-7突变体的干细胞发育缺陷的新抑制因素。由于ACN-1零突变体在早期幼虫发育期间死亡，我们使用RNAi来表征ACN-1在C.秀丽隐杆煤层发育中的作用，并确定其与异形因素的互动，包括Let-7及其下游互动者 - Lin- 41，HBL-1和APL-1。我们证明，虽然ACN-1的RNAi敲低不足以使其自身造成异形缺陷，但ACN-1的丧失抑制了Let-7突变体的延迟表型，并增强了HBL-1的早熟表型，但不是LIN-41，突变体。相反，在幼虫发育期间振荡的ACN-1表达的模式被Lin-41突变体破坏，但不是由HBL-1突变体破坏。最后，我们表明ACN-1（RNAi）增强了由APL-1损失引起的Let-7抑制表型，Alzheimer疾病导致淀粉样蛋白前体蛋白（APP）的同源物，同时显着破坏APL-的表达1在L4幼虫阶段。总之，ACN-1与异化学基因相互作用，似乎在Let-7及其靶基因的下游起作用，包括LIN-41和APL-1。

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