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全基因组范围内洞察碳代谢物阻遏蛋白(Cre1)对[昆虫病原菌名称]昆虫致病生命周期的深远影响 。 需注意,原文中“.”处应补充具体的昆虫病原菌名称,翻译才完整准确。

Genome-Wide Insight into Profound Effect of Carbon Catabolite Repressor (Cre1) on the Insect-Pathogenic Lifecycle of .

作者信息

Mohamed Rehab Abdelmonem, Ren Kang, Mou Ya-Ni, Ying Sheng-Hua, Feng Ming-Guang

机构信息

MOE Laboratory of Biosystems Homeostasis & Protection, College of Life Sciences, Zhejiang University, Hangzhou 310058, China.

出版信息

J Fungi (Basel). 2021 Oct 23;7(11):895. doi: 10.3390/jof7110895.

DOI:10.3390/jof7110895
PMID:34829184
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8622151/
Abstract

Carbon catabolite repression (CCR) is critical for the preferential utilization of glucose derived from environmental carbon sources and regulated by carbon catabolite repressor A (Cre1/CreA) in filamentous fungi. However, a role of Cre1-mediated CCR in insect-pathogenic fungal utilization of host nutrients during normal cuticle infection (NCI) and hemocoel colonization remains explored insufficiently. Here, we report an indispensability of Cre1 for 's utilization of nutrients in insect integument and hemocoel. Deletion of resulted in severe defects in radial growth on various media, hypersensitivity to oxidative stress, abolished pathogenicity via NCI or intrahemocoel injection (cuticle-bypassing infection) but no change in conidial hydrophobicity and adherence to insect cuticle. Markedly reduced biomass accumulation in the Δ cultures was directly causative of severe defect in aerial conidiation and reduced secretion of various cuticle-degrading enzymes. The majority (1117) of 1881 dysregulated genes identified from the Δ versus wild-type cultures were significantly downregulated, leading to substantial repression of many enriched function terms and pathways, particularly those involved in carbon and nitrogen metabolisms, cuticle degradation, antioxidant response, cellular transport and homeostasis, and direct/indirect gene mediation. These findings offer a novel insight into profound effect of Cre1 on the insect-pathogenic lifestyle of .

摘要

碳分解代谢物阻遏(CCR)对于优先利用源自环境碳源的葡萄糖至关重要,并且在丝状真菌中受碳分解代谢物阻遏蛋白A(Cre1/CreA)调控。然而,Cre1介导的CCR在昆虫病原真菌正常角质层感染(NCI)和血腔定殖过程中对宿主营养物质的利用方面所起的作用仍未得到充分研究。在此,我们报告了Cre1对于[真菌名称]在昆虫体表和血腔中利用营养物质的不可或缺性。[真菌名称]的缺失导致在各种培养基上的径向生长出现严重缺陷,对氧化应激超敏,通过NCI或血腔内注射(绕过角质层感染)的致病性丧失,但分生孢子疏水性和对昆虫角质层的粘附性没有变化。Δ[真菌名称]培养物中生物量积累的显著减少直接导致气生分生孢子形成严重缺陷以及各种角质层降解酶的分泌减少。从Δ[真菌名称]与野生型培养物中鉴定出的1881个失调基因中的大多数(1117个)显著下调,导致许多富集的功能术语和途径受到实质性抑制,特别是那些参与碳和氮代谢、角质层降解、抗氧化反应、细胞运输和稳态以及直接/间接基因介导的途径。这些发现为Cre1对[真菌名称]昆虫致病生活方式的深远影响提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b4/8622151/d7e70345cce6/jof-07-00895-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b4/8622151/c8aa2015e8e7/jof-07-00895-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b4/8622151/a7135882d73f/jof-07-00895-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b4/8622151/d2790575f6c8/jof-07-00895-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b4/8622151/1d9ff2fd9082/jof-07-00895-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b4/8622151/d7e70345cce6/jof-07-00895-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b4/8622151/c8aa2015e8e7/jof-07-00895-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b4/8622151/a7135882d73f/jof-07-00895-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b4/8622151/d2790575f6c8/jof-07-00895-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b4/8622151/1d9ff2fd9082/jof-07-00895-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b4/8622151/d7e70345cce6/jof-07-00895-g005.jpg

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