Cyclic Di-GMP Modulates the Disease Progression of Erwinia amylovora

Cyclic Di-GMP Modulates the Disease Progression of Erwinia amylovora
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DOI:
10.1128/jb.02068-12
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发表时间:
2013-05-01
影响因子:
3.2
通讯作者:
Waters, Christopher M.
Waters, Christopher M.
中科院分区:
生物学3区
文献类型:
--
作者:
Edmunds, Adam C.;Castiblanco, Luisa F.;Waters, Christopher M.

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第二信使环二GMP(c-di-GMP)是一种几乎普遍存在的细胞内信号分子,已知其调节各种细胞过程,包括生物膜形成、运动性和毒力。c-di-GMP的细胞内浓度由分别合成和降解c-di-GMP的二鸟苷酸环化酶(DGC)和磷酸二酯酶(PDE)负调控。c-di-GMP在植物火疫病病原菌和致病因子中的作用以前没有研究过。在这里,我们证明了五个预测的DGC基因在E。amylovora(edc基因,用于欧文氏菌二鸟苷酸环化酶)、edcA、edcC和edcE是活性二鸟苷酸环化酶。我们发现,c-di-GMP正调控E. amylovora,amylovoran,导致增加的生物膜形成,并负调节鞭毛游泳运动。虽然amylovoran分泌和生物膜的形成是重要的植物木质部组织的定殖和系统性感染的发展,删除两个生物膜促进DGCs增加组织坏死的未成熟梨感染试验和苹果芽感染模型,表明c-di-GMP负调控毒力。此外,c-di-GMP抑制hrpA的表达,hrpA是编码III型分泌菌毛的主要结构成分的基因。我们的结果是第一个描述的作用,c-di-GMP在E。amylovora,并建议下调运动和III型分泌的c-di-GMP在感染过程中起着关键作用的协调发病机制。
The second messenger cyclic di-GMP (c-di-GMP) is a nearly ubiquitous intracellular signal molecule known to regulate various cellular processes, including biofilm formation, motility, and virulence. The intracellular concentration of c-di-GMP is inversely governed by diguanylate cyclase (DGC) enzymes and phosphodiesterase (PDE) enzymes, which synthesize and degrade c-di-GMP, respectively. The role of c-di-GMP in the plant pathogen and causal agent of fire blight disease Erwinia amylovora has not been studied previously. Here we demonstrate that three of the five predicted DGC genes in E. amylovora (edc genes, for Erwinia diguanylate cyclase), edcA, edcC, and edcE, are active diguanylate cyclases. We show that c-di-GMP positively regulates the secretion of the main exopolysaccharide in E. amylovora, amylovoran, leading to increased biofilm formation, and negatively regulates flagellar swimming motility. Although amylovoran secretion and biofilm formation are important for the colonization of plant xylem tissues and the development of systemic infections, deletion of the two biofilm-promoting DGCs increased tissue necrosis in an immature-pear infection assay and an apple shoot infection model, suggesting that c-di-GMP negatively regulates virulence. In addition, c-di-GMP inhibited the expression of hrpA, a gene encoding the major structural component of the type III secretion pilus. Our results are the first to describe a role for c-di-GMP in E. amylovora and suggest that downregulation of motility and type III secretion by c-di-GMP during infection plays a key role in the coordination of pathogenesis.