The cyclase-associated protein FgCap1 has both protein kinase A-dependent and -independent functions during deoxynivalenol production and plant infection in Fusarium graminearum
The cyclase-associated protein FgCap1 has both protein kinase A-dependent and -independent functions during deoxynivalenol production and plant infection in Fusarium graminearum
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环化酶相关蛋白 FgCap1 在禾谷镰刀菌脱氧雪腐镰刀菌烯醇生产和植物感染过程中具有蛋白激酶 A 依赖性和非依赖性功能
DOI：
10.1111/mpp.12540
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发表时间：
2018
影响因子：
4.9
通讯作者：
Jiang Cong
中科院分区：
文献类型：
--
作者：
Yin Tao;Zhang Qiang;Wang Jianhua;Liu Huiquan;Wang Chenfang;Xu Jin-Rong;Jiang Cong
禾谷镰刀菌是小麦赤霉病的病原菌，也是毛霉毒素脱氧雪腐镰刀菌烯醇(DON)的产生者。毛霉烯生物合成(Tri)基因的表达和DON的产生主要受cAMP-PKA途径和两个途径特异性转录因子(TRI6和TRI10)的调控。有趣的是，TRI6的缺失突变体显示出cAMP信号的几个组成部分的表达降低，包括FgCAP1腺苷结合蛋白基因，该基因尚未在功能上被鉴定。禾本科植物。在这项研究中，我们发现FgCap1与Fac1腺苷环化酶相互作用，FgCAP1的缺失降低了细胞内cAMP水平和PKA活性。Fgcap1缺失突变体在营养生长、分生孢子发生和植物侵染等方面存在缺陷。外源cAMP可抑制DON的产生和TRI基因的表达，表明FgCap1对DON的生物合成具有PKA依赖性的调控作用。野生型，但不是突变型，在DON产生的条件下，细胞内cAMP和FgCAP1的表达水平增加。此外，FgCAP1的启动子含有一个可能的Tri6结合位点，对于其在DON生物合成过程中的功能是重要的，但对于菌丝生长、分生孢子发生和致病是必不可少的。此外，FgCap1在菌丝顶端的皮质斑块上显示出肌动蛋白样的定位。磷酸化蛋白质组学分析证明FgCap1在S353发生了磷酸化。FgCAP1的S353A突变不影响其在营养生长、分生孢子形成和DON产生过程中的功能。然而，FgCAP1S353A等位基因的表达不能弥补FgCap1突变体在植物侵染中的缺陷，表明FgCap1在S353的磷酸化在致病过程中的重要性。综上所述，我们的结果表明，FgCAP1通过cAMP信号参与DON的产生，并受到TRI6的反馈调节，但S353处FgCap1的磷酸化可能与cAMP-PKA途径无关，因为S353A突变只影响植物侵染。
Fusarium graminearumis a causal agent of wheat scab and a producer of the trichothecene mycotoxin deoxynivalenol (DON). The expression of trichothecene biosynthesis (TRI) genes and DON production are mainly regulated by the cyclic adenosine monophosphate‐protein kinase A (cAMP‐PKA) pathway and two pathway‐specific transcription factors (TRI6andTRI10). Interestingly, deletion mutants ofTRI6show reduced expression of several components of cAMP signalling, including theFgCAP1adenylate‐binding protein gene that has not been functionally characterized inF. graminearum. In this study, we show that FgCap1 interacts with Fac1 adenylate cyclase and that deletion ofFgCAP1reduces the intracellular cAMP level and PKA activity. TheFgcap1deletion mutant is defective in vegetative growth, conidiogenesis and plant infection. It also shows significantly reduced DON production andTRIgene expression, which can be suppressed by exogenous cAMP, indicating a PKA‐dependent regulation of DON biosynthesis by FgCap1. The wild‐type, but nottri6mutant, shows increased levels of intracellular cAMP andFgCAP1expression under DON‐producing conditions. Furthermore, the promoter ofFgCAP1contains one putative Tri6‐binding site that is important for its function during DON biosynthesis, but is dispensable for hyphal growth, conidiogenesis and pathogenesis. In addition, FgCap1 shows an actin‐like localization to the cortical patches at the apical region of hyphal tips. Phosphorylation of FgCap1 at S353 was identified by phosphoproteomics analysis. The S353A mutation inFgCAP1has no effect on its functions during vegetative growth, conidiation and DON production. However, expression of theFgCAP1S353Aallele fails to complement the defects of theFgcap1mutant in plant infection, indicating the importance of the phosphorylation of FgCap1 at S353 during pathogenesis. Taken together, our results suggest thatFgCAP1is involved in the regulation of DON production via cAMP signalling and subjected to a feedback regulation byTRI6, but the phosphorylation of FgCap1 at S353 is probably unrelated to the cAMP‐PKA pathway because the S353A mutation only affects plant infection.