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缺失 Aspergillus nidulans 中的 celA 基因会触发次生代谢物生物合成基因的过度表达。

Deletion of the celA gene in Aspergillus nidulans triggers overexpression of secondary metabolite biosynthetic genes.

机构信息

Luxembourg Institute of Science and Technology (LIST), Environmental Research and Innovation (ERIN) Department, Esch/Alzette, L-4362, Luxembourg.

University of Natural Resources and Life Sciences Vienna (BOKU), Department of Applied Genetics and Cell Biology, Fungal Genetics and Genomics Unit, BOKU Campus, Tulln/Donau, A-3430, Austria.

出版信息

Sci Rep. 2017 Jul 20;7(1):5978. doi: 10.1038/s41598-017-05920-x.

DOI:10.1038/s41598-017-05920-x
PMID:28729615
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5519750/
Abstract

Although much progress has been made in the study of cell wall biosynthetic genes in the model filamentous fungus Aspergillus nidulans, there are still targets awaiting characterization. An example is the gene celA (ANIA_08444) encoding a putative mixed linkage glucan synthase. To characterize the role of celA, we deleted it in A. nidulans, analyzed the phenotype of the mycelium and performed RNA-Seq. The strain shows a very strong phenotype, namely "balloons" along the hyphae and aberrant conidiophores, as well as an altered susceptibility to cell wall drugs. These data suggest a potential role of the gene in cell wall-related processes. The Gene Ontology term Enrichment analysis shows increased expression of secondary metabolite biosynthetic genes (sterigmatocystin in particular) in the deleted strain. Our results show that the deletion of celA triggers a strong phenotype reminiscent of cell wall-related aberrations and the upregulation of some secondary metabolite gene clusters in A. nidulans.

摘要

尽管在模式丝状真菌构巢曲霉中细胞壁生物合成基因的研究已经取得了很大进展,但仍有一些目标有待表征。例如,celA 基因(ANIA_08444)编码一种假定的混合连接葡聚糖合酶。为了表征 celA 的作用,我们在构巢曲霉中删除了它,分析了菌丝体的表型并进行了 RNA-Seq 分析。该菌株表现出非常强的表型,即“气球”状沿菌丝体和异常的分生孢子梗,以及对细胞壁药物的敏感性改变。这些数据表明该基因在细胞壁相关过程中可能具有作用。基因本体论术语富集分析显示,缺失菌株中次级代谢物生物合成基因(特别是桔青霉素)的表达增加。我们的结果表明,celA 的缺失会触发类似于细胞壁相关异常的强烈表型,并上调构巢曲霉中一些次级代谢物基因簇的表达。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/327a/5519750/a87f2c2b3533/41598_2017_5920_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/327a/5519750/df585a9d6f5b/41598_2017_5920_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/327a/5519750/98a8e517039c/41598_2017_5920_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/327a/5519750/4305e5190667/41598_2017_5920_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/327a/5519750/111fd4d31465/41598_2017_5920_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/327a/5519750/6f4900f539f1/41598_2017_5920_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/327a/5519750/2640db4fd2be/41598_2017_5920_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/327a/5519750/a87f2c2b3533/41598_2017_5920_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/327a/5519750/df585a9d6f5b/41598_2017_5920_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/327a/5519750/98a8e517039c/41598_2017_5920_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/327a/5519750/4305e5190667/41598_2017_5920_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/327a/5519750/111fd4d31465/41598_2017_5920_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/327a/5519750/6f4900f539f1/41598_2017_5920_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/327a/5519750/2640db4fd2be/41598_2017_5920_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/327a/5519750/a87f2c2b3533/41598_2017_5920_Fig7_HTML.jpg

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