State Key Laboratory of North China Crop Improvement and Regulation, Baoding, China.
College of Life Sciences, Hebei Agricultural University, Baoding, China.
Mol Plant Pathol. 2022 Nov;23(11):1608-1619. doi: 10.1111/mpp.13253. Epub 2022 Aug 5.
The cyclic adenosine monophosphate (cAMP) signalling pathway plays an important role in the regulation of the development and pathogenicity of filamentous fungi. cAMP-dependent protein kinase A (PKA) is the conserved element downstream of cAMP, and its diverse mechanisms in multiple filamentous fungi are not well known yet. In the present study, gene knockout mutants of two catalytic subunits of PKA (PKA-C) in Setosphaeria turcica were created to illustrate the regulatory mechanisms of PKA-Cs on the development and pathogenicity of S. turcica. As a result, StPkaC2 was proved to be the main contributor of PKA activity in S. turcica. In addition, it was found that both StPkaC1 and StPkaC2 were necessary for conidiation and invasive growth, while only StPkaC2 played a negative role in the regulation of filamentous growth. We reveal that only StPkaC2 could interact with the transcription factor StEfg1, and it inhibited the transcription of StRAB1, a Rab GTPase homologue coding gene in S. turcica, whereas StPkaC1 could specifically interact with a transcriptional regulator StFlo8, which could rescue the transcriptional inhibition of StEfg1 on StRAB1. We also demonstrated that StRAB1 could positively influence the biosynthesis of chitin in hyphae, thus changing the filamentous growth. Our findings clarify that StPkaC2 participates in chitin biosynthesis to modulate mycelium development by targeting the Efg1-mediated transcription of StRAB1, while StFlo8, interacting with StPkaC1, acts as a negative regulator during this process.
环腺苷酸(cAMP)信号通路在丝状真菌的发育和致病性调节中起着重要作用。cAMP 依赖性蛋白激酶 A(PKA)是 cAMP 的下游保守成分,其在多种丝状真菌中的多种机制尚不清楚。在本研究中,通过创建 Setosphaeria turcica 中两个 PKA 催化亚基(PKA-C)的基因敲除突变体,阐明了 PKA-Cs 对 S. turcica 发育和致病性的调节机制。结果表明,StPkaC2 是 S. turcica 中 PKA 活性的主要贡献者。此外,发现 StPkaC1 和 StPkaC2 都对分生孢子形成和侵袭性生长是必要的,而只有 StPkaC2 对丝状生长的调节起负作用。我们揭示了只有 StPkaC2 才能与转录因子 StEfg1 相互作用,并且它抑制了 S. turcica 中 Rab GTPase 同源物编码基因 StRAB1 的转录,而 StPkaC1 可以特异性地与转录调节剂 StFlo8 相互作用,StFlo8 可以挽救 StEfg1 对 StRAB1 的转录抑制。我们还证明了 StRAB1 可以正向影响菌丝中几丁质的生物合成,从而改变丝状生长。我们的研究结果阐明了 StPkaC2 通过靶向 Efg1 介导的 StRAB1 转录参与几丁质生物合成来调节菌丝体发育,而与 StPkaC1 相互作用的 StFlo8 在这个过程中充当负调节剂。