NikA/TcsC histidine kinase is involved in conidiation, hyphal morphology, and responses to osmotic stress and antifungal chemicals in Aspergillus fumigatus.
NikA/TcsC histidine kinase is involved in conidiation, hyphal morphology, and responses to osmotic stress and antifungal chemicals in Aspergillus fumigatus.
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Nika/TCSC组氨酸激酶参与曲曲霉中对渗透胁迫和抗真菌化学物质的菌丝形态和反应。
DOI：
10.1371/journal.pone.0080881
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Kawamoto S
中科院分区：
文献类型：
--
作者：
Hagiwara D;Takahashi-Nakaguchi A;Toyotome T;Yoshimi A;Abe K;Kamei K;Gonoi T;Kawamoto S
真菌高渗甘油（HOG）途径由双组分系统（TCS）和Hog 1型丝裂原活化蛋白激酶（MAPK）级联组成。第III组（Nik 1型）组氨酸激酶在几种丝状真菌的HOG途径中起着重要作用。在这项研究中，我们的特点是第三组组氨酸激酶，NikA/TcsC，在危及生命的致病真菌，烟曲霉。nikA的缺失突变体表现出分生孢子产量低，菌丝异常，对高渗透压胁迫显着敏感，对细胞壁扰动试剂如刚果红和calcofluor白色，以及杀菌剂如咯菌腈，异菌脲和硝吡咯菌素具有抗性。在SskA反应调节子和SakA MAPK的突变体中没有观察到这些表型，它们被认为是NikA的下游组分。与此相反，在咯菌腈处理的反应中，NikA参与了SakA MAPK的磷酸化和catA、dprA和dprB的转录上调，这些都是在SakA的控制下调节的。然后，我们测试了不仅NikA，而且其他13种组氨酸激酶在HOG途径的调节中发挥一定作用的想法。有趣的是，fos 1，phkA，phkB，fhk 5，和fhk 6的表达增加渗透压休克或咯菌腈处理在SakA依赖的方式。然而，组氨酸激酶的缺失突变体在测试条件下的生长没有显示出显著的缺陷。总的来说，尽管NikA相关的信号转导网络看似复杂，但NikA在A.烟曲霉生理学，并在一定程度上调节HOG途径。
The fungal high osmolarity glycerol (HOG) pathway is composed of a two-component system (TCS) and Hog1-type mitogen-activated protein kinase (MAPK) cascade. A group III (Nik1-type) histidine kinase plays a major role in the HOG pathway of several filamentous fungi. In this study, we characterized a group III histidine kinase, NikA/TcsC, in the life-threatening pathogenic fungus, Aspergillus fumigatus. A deletion mutant of nikA showed low conidia production, abnormal hyphae, marked sensitivity to high osmolarity stresses, and resistance to cell wall perturbing reagents such as congo red and calcofluor white, as well as to fungicides such as fludioxonil, iprodione, and pyrrolnitrin. None of these phenotypes were observed in mutants of the SskA response regulator and SakA MAPK, which were thought to be downstream components of NikA. In contrast, in response to fludioxonil treatment, NikA was implicated in the phosphorylation of SakA MAPK and the transcriptional upregulation of catA, dprA, and dprB, which are regulated under the control of SakA. We then tested the idea that not only NikA, but also the other 13 histidine kinases play certain roles in the regulation of the HOG pathway. Interestingly, the expression of fos1, phkA, phkB, fhk5, and fhk6 increased by osmotic shock or fludioxonil treatment in a SakA-dependent manner. However, deletion mutants of the histidine kinases showed no significant defects in growth under the tested conditions. Collectively, although the signal transduction network related to NikA seems complicated, NikA plays a crucial role in several aspects of A. fumigatus physiology and, to a certain extent, modulates the HOG pathway.
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