five

Dataset for: Ifu5, a WW domain-containing protein interacts with Efg1 to achieve coordination of normoxic and hypoxic functions to influence pathogenicity traits in <i>Candida albicans</i>

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DataCite Commons2020-08-26 更新2024-07-27 收录
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https://wiley.figshare.com/articles/Dataset_for_Ifu5_a_WW_domain-containing_protein_interacts_with_Efg1_to_achieve_coordination_of_normoxic_and_hypoxic_functions_to_influence_pathogenicity_traits_in_i_Candida_albicans_i_/10115927/1
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资源简介:
Hypoxic adaptation pathways, essential for <i>Candida albicans</i> pathogenesis, are tied to its transition from a commensal to a pathogen. Herein, we identify a WW domain-containing protein, Ifu5, as a determinant of hypoxic adaptation that also impacts normoxic responses in this fungus. Ifu5 activity supports glycosylation homeostasis via the Cek1 MAP kinase-dependent upregulation of <i>PMT1</i>, under normoxia. Transcriptome analysis of <i>ifu5</i>Δ/Δ under normoxia shows a significant upregulation of the hypoxic regulator <i>EFG1</i> and -dependent genes. We demonstrate physical interaction between Ifu5 by virtue of its WW domain and Efg1 that represses <i>EFG1</i> expression under normoxia. This interaction is lost under hypoxic growth conditions, relieving <i>EFG1</i> repression. Hypoxic adaptation processes such as filamentation and biofilm formation are affected in <i>ifu5</i>Δ/Δ cells revealing the role of Ifu5 in hypoxic signalling and modulating pathogenicity traits of <i>C. albicans</i> under varied oxygen conditions. Additionally, the WW domain of Ifu5 facilitates its role in hypoxic adaptation, revealing the importance of this domain in providing a platform to integrate various cellular processes. These data forge a relationship between Efg1 and Ifu5 that fosters the role of Ifu5 in hypoxic adaptation, thus illuminating novel strategies to undermine the growth of <i>C. albicans</i>.

缺氧适应通路对于白色念珠菌(Candida albicans)的致病过程至关重要,且与其从共生菌向致病菌的转变密切相关。本研究鉴定出一种含WW结构域(WW domain)的蛋白Ifu5,其既是缺氧适应的调控因子,同时也影响该真菌的常氧应答。在常氧条件下,Ifu5通过依赖于Cek1丝裂原活化蛋白激酶(MAP kinase)的途径上调PMT1基因的表达,以此维持糖基化稳态。对ifu5Δ/Δ缺失突变体的常氧转录组分析显示,缺氧调控因子EFG1及其下游依赖基因出现显著上调。研究证实,Ifu5可通过其WW结构域与Efg1发生物理互作,在常氧条件下抑制EFG1基因的表达;而在缺氧培养条件下,该互作消失,解除了对EFG1的转录抑制。ifu5Δ/Δ缺失突变体的缺氧适应过程(如菌丝形成与生物被膜形成)受到显著影响,揭示了Ifu5在缺氧信号通路中的作用,并可调控不同氧浓度条件下白色念珠菌的致病相关性状。此外,Ifu5的WW结构域介导了其在缺氧适应中的功能,表明该结构域可作为整合多种细胞生理过程的平台,其功能具有重要意义。本研究揭示了Efg1与Ifu5之间的调控关系,明确了Ifu5在缺氧适应中的核心作用,从而为抑制白色念珠菌的增殖提供了全新的干预策略。
提供机构:
Wiley
创建时间:
2019-11-18
搜集汇总
数据集介绍
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背景与挑战
背景概述
该数据集支持白色念珠菌中Ifu5蛋白与Efg1相互作用的研究,揭示了Ifu5通过WW结构域协调常氧和缺氧功能,影响菌株的致病性特征,如菌丝形成和生物膜发育。数据来源于转录组分析,旨在阐明缺氧适应机制,为抗真菌策略提供新见解。
以上内容由遇见数据集搜集并总结生成
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