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编码一种低亲和力的环磷酸腺苷磷酸二酯酶,调控柑橘致病型中的分生孢子形成和致病性。

, Encoding a Low-Affinity cAMP Phosphodiesterase, Regulates Conidiation and Pathogenesis in Tangerine Pathotype.

作者信息

Lv Weiwei, Kong Xiangwen, Zhou Changyong, Tang Kezhi

机构信息

Citrus Research Institute, Southwest University, Chongqing, China.

出版信息

Front Microbiol. 2020 Dec 7;11:597545. doi: 10.3389/fmicb.2020.597545. eCollection 2020.

DOI:10.3389/fmicb.2020.597545
PMID:33365022
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7750186/
Abstract

Based on intracellular second messenger cAMP, the cyclic AMP-protein kinase A (cAMP-PKA) pathway transforms extracellular stimuli to activate effectors and downstream signaling components, mediating physiological processes in filamentous fungi. The concentration of intracellular cAMP was regulated by adenylate cyclase biosynthesis and cAMP phosphodiesterase (PDEs) hydrolysis, which mediate signal transduction and termination. In this study, we used a gene deletion and complementary strategy to characterize the functions of and genes, which encoded low-affinity PDEs (Pdel) and high-affinity PDEs (Pdeh), respectively, in , but not , was found to be a key regulator in conidiation and pathogenesis in . Δ showed defects in conidiation, producing approximately 65% reduced conidiation and forming lowly pigmented aberrant structures. In response to osmotic stress, Δ was more sensitive to non-ionic osmotic stress than ionic osmotic stress. Moreover, deletion mutants had defects in vegetative growth and hyphal growth. Further analyses showed that the high chitin content of Δ might account for the sensitivity to Congo red. Based on the attenuated pathogenicity and lowly pigmented aberrant structures, the laccase activity analysis found that both and were involved in laccase activity regulation. Our data further support the PKA-mediated cAMP signaling pathway, as we have found that was involved in intracellular cAMP levels in

摘要

基于细胞内第二信使环磷酸腺苷(cAMP),环磷酸腺苷-蛋白激酶A(cAMP-PKA)途径将细胞外刺激转化为激活效应器和下游信号成分,介导丝状真菌的生理过程。细胞内cAMP的浓度由腺苷酸环化酶生物合成和cAMP磷酸二酯酶(PDEs)水解调节,二者分别介导信号转导和终止。在本研究中,我们采用基因缺失和互补策略来表征分别编码低亲和力PDEs(Pdel)和高亲和力PDEs(Pdeh)的 和 基因的功能,发现 而非 是 分生孢子形成和致病过程中的关键调节因子。Δ 在分生孢子形成方面存在缺陷,分生孢子产量降低约65%,并形成色素沉着较浅的异常结构。在渗透胁迫下,Δ 对非离子渗透胁迫比离子渗透胁迫更敏感。此外, 缺失突变体在营养生长和菌丝生长方面存在缺陷。进一步分析表明,Δ 中几丁质含量高可能是其对刚果红敏感的原因。基于致病性减弱和色素沉着较浅的异常结构,漆酶活性分析发现 和 均参与漆酶活性调节。我们的数据进一步支持了PKA介导的cAMP信号通路,因为我们发现 在 中参与细胞内cAMP水平调节

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28d7/7750186/4fcfd1699dc8/fmicb-11-597545-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28d7/7750186/dbb231244184/fmicb-11-597545-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28d7/7750186/aa8c401da852/fmicb-11-597545-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28d7/7750186/ee927194f561/fmicb-11-597545-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28d7/7750186/4fcfd1699dc8/fmicb-11-597545-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28d7/7750186/dbb231244184/fmicb-11-597545-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28d7/7750186/fb094496e7dd/fmicb-11-597545-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28d7/7750186/c7db183d724b/fmicb-11-597545-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28d7/7750186/8bc3e458a8b8/fmicb-11-597545-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28d7/7750186/aa8c401da852/fmicb-11-597545-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28d7/7750186/ee927194f561/fmicb-11-597545-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28d7/7750186/4fcfd1699dc8/fmicb-11-597545-g007.jpg

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Cell-Wall-Degrading Enzymes Required for Virulence in the Host Selective Toxin-Producing Necrotroph of Citrus.
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The cAMP/Protein Kinase a Pathway Regulates Virulence and Adaptation to Host Conditions in .环磷酸腺苷/蛋白激酶 A 途径调节 在 中的毒力和对宿主条件的适应。
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