Jöhnk Bastian, Bayram Özgür, Abelmann Anja, Heinekamp Thorsten, Mattern Derek J, Brakhage Axel A, Jacobsen Ilse D, Valerius Oliver, Braus Gerhard H
Department of Molecular Microbiology and Genetics and Göttingen Center for Molecular Biosciences (GZMB), Georg-August-University, Göttingen, Germany.
Department of Biology, Maynooth University, National University of Ireland, Maynooth, County Kildare, Ireland.
PLoS Pathog. 2016 Sep 20;12(9):e1005899. doi: 10.1371/journal.ppat.1005899. eCollection 2016 Sep.
F-box proteins share the F-box domain to connect substrates of E3 SCF ubiquitin RING ligases through the adaptor Skp1/A to Cul1/A scaffolds. F-box protein Fbx15 is part of the general stress response of the human pathogenic mold Aspergillus fumigatus. Oxidative stress induces a transient peak of fbx15 expression, resulting in 3x elevated Fbx15 protein levels. During non-stress conditions Fbx15 is phosphorylated and F-box mediated interaction with SkpA preferentially happens in smaller subpopulations in the cytoplasm. The F-box of Fbx15 is required for an appropriate oxidative stress response, which results in rapid dephosphorylation of Fbx15 and a shift of the cellular interaction with SkpA to the nucleus. Fbx15 binds SsnF/Ssn6 as part of the RcoA/Tup1-SsnF/Ssn6 co-repressor and is required for its correct nuclear localization. Dephosphorylated Fbx15 prevents SsnF/Ssn6 nuclear localization and results in the derepression of gliotoxin gene expression. fbx15 deletion mutants are unable to infect immunocompromised mice in a model for invasive aspergillosis. Fbx15 has a novel dual molecular function by controlling transcriptional repression and being part of SCF E3 ubiquitin ligases, which is essential for stress response, gliotoxin production and virulence in the opportunistic human pathogen A. fumigatus.
F-box蛋白共享F-box结构域,通过接头蛋白Skp1/A与Cul1/A支架连接E3 SCF泛素RING连接酶的底物。F-box蛋白Fbx15是人类致病霉菌烟曲霉一般应激反应的一部分。氧化应激诱导fbx15表达出现短暂峰值,导致Fbx15蛋白水平升高3倍。在非应激条件下,Fbx15被磷酸化,F-box介导的与SkpA的相互作用优先发生在细胞质中较小的亚群中。Fbx15的F-box对于适当的氧化应激反应是必需的,这导致Fbx15快速去磷酸化,并使细胞与SkpA的相互作用转移到细胞核。Fbx15作为RcoA/Tup1-SsnF/Ssn6共抑制因子的一部分与SsnF/Ssn6结合,并且是其正确核定位所必需的。去磷酸化的Fbx15阻止SsnF/Ssn6的核定位,并导致麦角硫因基因表达的去抑制。在侵袭性曲霉病模型中,fbx15缺失突变体无法感染免疫受损小鼠。Fbx15通过控制转录抑制以及作为SCF E3泛素连接酶的一部分具有一种新的双重分子功能,这对于机会性人类病原体烟曲霉的应激反应、麦角硫因产生和毒力至关重要。