Shah Rashmi, Pathak Gopal, Drepper Thomas, Gärtner Wolfgang
Max-Planck-Institute for Chemical Energy Conversion, Mülheim, Germany.
Institute of Molecular Enzyme Technology, Heinrich Heine University Düsseldorf, Forschungszentrum Jülich, Jülich, Germany.
Photochem Photobiol. 2016 Jul;92(4):571-8. doi: 10.1111/php.12610.
The plant pathogen Pseudomonas syringae (Ps) is a well-established model organism for bacterial infection of plants. The genome sequences of two pathovars, pv. syringae and pv. tomato, revealed one gene encoding a blue and two genes encoding red/far red light-sensing photoreceptors. Continuing former molecular characterization of the photoreceptor proteins, we here report selective photoreceptor gene disruption for pv. tomato aiming at identification of potentially regulatory functions of these photoreceptors. Transformation of Ps cells with linear DNA constructs yielded interposon mutations of the corresponding genes. Cell growth studies of the generated photoreceptor knock-out mutants revealed their role in light-dependent regulation of cell growth and motility. Disruption of the blue-light (BL) receptor gene caused a growth deregulation, in line with an observed increased virulence of this mutant (Moriconi et al., Plant J., 2013, 76, 322). Bacterial phytochrome-1 (BphP1) deletion mutant caused unaltered cell growth, but a stronger swarming capacity. Inactivation of its ortholog, BphP2, however, caused reduced growth and remarkably altered dendritic swarming behavior. Combined knock-out of both bacteriophytochromes reproduced the swarming pattern observed for the BphP2 mutant alone. A triple knock-out mutant showed a growth rate between that of the BL (deregulation) and the phytochrome-2 mutant (growth reduction).
植物病原体丁香假单胞菌（Ps）是植物细菌感染方面成熟的模式生物。两个致病变种pv. syringae和pv. tomato的基因组序列显示，有一个基因编码蓝光感光受体，两个基因编码红光/远红光感光受体。延续之前对感光受体蛋白的分子特征研究，我们在此报告针对pv. tomato的选择性感光受体基因破坏，旨在确定这些感光受体的潜在调控功能。用线性DNA构建体转化Ps细胞产生了相应基因的转座子突变。对所产生的感光受体敲除突变体的细胞生长研究揭示了它们在细胞生长和运动的光依赖性调控中的作用。蓝光（BL）受体基因的破坏导致生长失调，这与该突变体观察到的毒力增加一致（莫里科尼等人，《植物杂志》，2013年，76卷，322页）。细菌光敏色素-1（BphP1）缺失突变体导致细胞生长未改变，但群体运动能力增强。然而，其直系同源物BphP2的失活导致生长减少和显著改变的树枝状群体运动行为。两种细菌光敏色素的联合敲除重现了单独BphP2突变体观察到的群体运动模式。三重敲除突变体的生长速率介于BL（失调）和光敏色素-2突变体（生长减少）之间。
