Department of Biological Sciences, University of Wisconsin-Milwaukee, Milwaukee, Wisconsin, USA.
National Center for Cool and Cold Water Aquaculture, Agricultural Research Service, USDA, Kearneysville, West Virginia, USA.
J Bacteriol. 2024 Apr 18;206(4):e0006824. doi: 10.1128/jb.00068-24. Epub 2024 Mar 22.
causes columnaris disease in fish. Columnaris disease is incompletely understood, and adequate control measures are lacking. The type IX secretion system (T9SS) is required for gliding motility and virulence. The T9SS and gliding motility machineries share some, but not all, components. GldN (required for gliding and for secretion) and PorV (involved in secretion but not required for gliding) are both needed for virulence, implicating T9SS-mediated secretion in virulence. The role of motility in virulence is uncertain. We constructed and analyzed , , and mutants that were defective for motility but that maintained T9SS function to understand the role of motility in virulence. Wild-type cells moved rapidly and formed spreading colonies. In contrast, and deletion mutants were partially defective in gliding and formed nonspreading colonies. Both mutants exhibited reduced virulence in rainbow trout fry. A deletion mutant was nonmotile, secretion deficient, and avirulent in rainbow trout fry. To separate the roles of GldJ in secretion and in motility, we generated truncation mutants that produce nearly full-length GldJ. Mutant , which produces GldJ truncated at amino acid 563, was defective for gliding but was competent for secretion as measured by extracellular proteolytic activity. This mutant displayed reduced virulence in rainbow trout fry, suggesting that motility contributes to virulence. Fish that survived exposure to the deletion mutant or the mutant exhibited partial resistance to later challenge with wild-type cells. The results aid our understanding of columnaris disease and may suggest control strategies.IMPORTANCE causes columnaris disease in many species of freshwater fish in the wild and in aquaculture systems. Fish mortalities resulting from columnaris disease are a major problem for aquaculture. virulence is incompletely understood, and control measures are inadequate. Gliding motility and protein secretion have been suggested to contribute to columnaris disease, but evidence directly linking motility to disease was lacking. We isolated and analyzed mutants that were competent for secretion but defective for motility. Some of these mutants exhibited decreased virulence. Fish that had been exposed to these mutants were partially protected from later exposure to the wild type. The results contribute to our understanding of columnaris disease and may aid development of control strategies.
在鱼类中引起柱状病。柱状病的发病机制尚不完全清楚，也缺乏有效的控制措施。IX 型分泌系统（T9SS）是滑行运动和毒力所必需的。T9SS 和滑行运动机械具有一些共同的成分，但并非全部。GldN（滑行和分泌所必需）和 PorV（参与分泌但滑行不需要）对毒力都是必需的，这表明 T9SS 介导的分泌与毒力有关。运动在毒力中的作用尚不确定。我们构建并分析了滑行运动缺陷但 T9SS 功能保持的 、 和 突变体，以了解运动在毒力中的作用。野生型细胞快速移动并形成扩散菌落。相比之下， 和 缺失突变体在滑行运动中部分缺陷，并形成非扩散菌落。这两个突变体在彩虹鳟鱼苗中的毒力都降低了。 缺失突变体在彩虹鳟鱼苗中不运动、不分泌、无致病性。为了将 GldJ 在分泌和运动中的作用分开，我们生成了产生几乎全长 GldJ 的 截断突变体。突变体 ，其产生截断在 563 个氨基酸的 GldJ，在滑行运动中缺陷，但如通过细胞外蛋白水解活性测量，在分泌方面是有能力的。这种突变体在彩虹鳟鱼苗中的毒力降低，表明运动有助于毒力。暴露于 缺失突变体或 突变体的鱼对随后用野生型细胞进行的挑战表现出部分抗性。结果有助于我们理解柱状病，并可能提出控制策略。重要的是，在野外和水产养殖系统中，在许多淡水鱼类物种中引起柱状病。由柱状病引起的鱼类死亡率是水产养殖的一个主要问题。柱状病的毒力机制尚不完全清楚，控制措施也不足。滑行运动和蛋白分泌被认为与柱状病有关，但缺乏将运动直接与疾病联系起来的证据。我们分离并分析了滑行运动缺陷但分泌能力正常的突变体。其中一些突变体的毒力降低。暴露于这些突变体的鱼对随后暴露于野生型的部分保护。结果有助于我们理解柱状病，并可能有助于开发控制策略。
