Motility is required for many bacterial pathogens to reach and colonize target sites. Vibrio cholerae traverses a thick mucus barrier coating the small intestine to reach the underlying epithelium. We screened a transposon library in motility medium containing mucin to identify factors that influence mucus transit. Lesions in structural genes of the type VI secretion system (T6SS) were among those recovered. Two-dimensional (2D) and 3D single-cell tracking was used to compare the motility behaviors of wild-type cells and a mutant that collectively lacked three essential T6SS structural genes (T6SS⁻). In the absence of mucin, wild-type and T6SS⁻ cells exhibited similar speeds and run-reverse-flick (RRF) swimming patterns, in which forward-moving cells briefly backtrack before stochastically reorienting (flicking) in a new direction upon resuming forward movement. We show that mucin induced T6SS expression and activity in wild-type bacteria but significantly decreased their swimming speed and flicking, yielding curvilinear or near-surface circular traces for many cells. Conversely, mucin slowed T6SS⁻ cells to a lesser extent, and many continued to flick and produce RRF-like traces. ΔcheY3 cells, which exclusively swim in the forward direction and thus cannot flick, also produced curvilinear traces with or without mucin present and, on occasion, near-surface circular traces in the presence of mucin. The dependence of flicking on swimming speed suggested that mucin-induced T6SS activity further decreased V. cholerae motility and thereby reduced flicking probability during reverse-to-forward transitions. We propose that this encourages cells to continue on their current trajectory rather than reorienting, which may benefit those tracking toward the epithelial surface.

中文翻译：

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霍乱弧菌的VI型活性改变了粘蛋白的运动行为。

许多细菌性病原体到达并定居目标部位需要动力。霍乱弧菌穿过厚厚的粘液屏障，覆盖小肠，到达下层上皮。我们在含有粘蛋白的动力培养基中筛选了一个转座子文库，以鉴定影响粘液转运的因素。VI型分泌系统（T6SS）的结构基因中的病灶已恢复。二维（2D）和三维单细胞跟踪被用于比较的野生型细胞的运动行为和突变共同缺乏三个基本T6SS结构基因（T6SS ^- ）。在没有粘蛋白，野生型和T6SS的情况下^-细胞表现出相似的速度和逆跳运动（RRF）游动模式，其中向前移动的细胞会短暂地向后退，然后在恢复向前移动时以新的方向随机重新定向（滑动）。我们显示粘蛋白诱导野生型细菌中的T6SS表达和活性，但显着降低了它们的游泳速度和甩动，对许多细胞产生了曲线或近表面的圆形痕迹。相反地，粘蛋白减慢T6SS ^-细胞在较小程度上，以及许多继续轻拂和农产品RRF状痕迹。Δ cheY3仅在向前方向游动并因此不能弹动的细胞还会在存在或不存在粘蛋白的情况下产生曲线痕迹，有时还会在存在粘蛋白的情况下产生近表面的圆形痕迹。甩动对游泳速度的依赖性表明，粘蛋白诱导的T6SS活性进一步降低了霍乱弧菌的运动能力，从而降低了从前向后过渡期间的甩动概率。我们建议这鼓励细胞继续沿其当前轨迹而不是重新定向，这可能有益于那些朝着上皮表面跟踪的人。