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烟曲霉组 III 混合组氨酸激酶 TcsC 和构巢曲霉 NikA 的功能比较。

Functional comparison of the group III hybrid histidine kinases TcsC of Aspergillus fumigatus and NikA of Aspergillus nidulans.

机构信息

Institute for Infectious Diseases and Zoonoses, Ludwig-Maximilians-University, Munich, Germany.

出版信息

Med Mycol. 2020 Apr 1;58(3):362-371. doi: 10.1093/mmy/myz069.

Abstract

In filamentous fungi, group III hybrid histidine kinases (HHKs) are major and nonredundant sensing proteins of the high osmolarity glycerol pathway. In this study, we have compared the biological functions of the two homologous group III HHKs TcsC of Aspergillus fumigatus and NikA of A. nidulans. As expected from previous studies, the corresponding mutants are severely impaired in their ability to adapt to hyperosmotic stress and are both resistant to the antifungal agent fludioxonil. However, our data also reveal novel phenotypes and differences between these mutants. Both TcsC and NikA are required for wild-type-like growth on Czapek-Dox medium and a normal resistance to certain oxidative stressors, whereas an increased resistance to the cell wall disturbing agents Congo red and Calcofluor white was found for the ΔtcsC but not for the ΔnikA mutant. With respect to the cell wall reorganizations that are triggered by fludioxonil in a TcsC/NikA-dependent manner, we observed similarities but also striking differences. Strains from seven Aspergillus species, including A. fumigatus and A. nidulans incorporated more chitin into their cell walls in response to fludioxonil. In contrast, fludioxonil treatment resulted in a shedding of surface accessible galactomannan and β-1,3-glucan in all Aspergillus strains tested except A. nidulans. Hence, the fludioxonil-induced activation of NikA results in a distinct and apparently A. nidulans-specific pattern of cell wall reorganizations that is not due to NikA itself, but its integration into the A. nidulans signaling network.

摘要

在丝状真菌中,第三组混合组氨酸激酶(HHK)是高渗甘油途径的主要且非冗余感应蛋白。在这项研究中,我们比较了烟曲霉 TcsC 和构巢曲霉 NikA 这两种同源的第三组 HHK 的生物学功能。正如先前研究所预期的那样,相应的突变体在适应高渗胁迫的能力上受到严重损害,并且对杀真菌剂氟啶酮都有抗性。然而,我们的数据还揭示了这些突变体之间的新表型和差异。TcsC 和 NikA 都需要野生型样的 Czapek-Dox 培养基上的生长和对某些氧化应激因子的正常抗性,而ΔtcsC 对细胞壁干扰剂刚果红和 Calcofluor white 的抗性增加,但ΔnikA 突变体没有。对于 TcsC/NikA 依赖性触发的细胞壁重排,我们观察到相似之处,但也有明显的差异。包括烟曲霉和构巢曲霉在内的七种曲霉属菌株对 fludioxonil 的反应是将更多的几丁质掺入细胞壁中。相比之下,除了构巢曲霉之外,所有测试的曲霉属菌株在 fludioxonil 处理后都会脱落表面可及的半乳糖甘露聚糖和β-1,3-葡聚糖。因此,NikA 的氟啶酮诱导激活导致了一种明显的、显然是构巢曲霉特异性的细胞壁重排模式,这不是由于 NikA 本身,而是由于其整合到构巢曲霉的信号网络中。

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