Dhasmana Neha, Kumar Nishant, Gangwal Aakriti, Keshavam Chetkar Chandra, Singh Lalit K, Sangwan Nitika, Nashier Payal, Biswas Sagarika, Pomerantsev Andrei P, Leppla Stephen H, Singh Yogendra, Gupta Meetu
CSIR-Institute of Genomics and Integrative Biology, Mall Road, Delhi, India.
Academy of Scientific and Innovative Research (AcSIR), Ghaziabad- 201002, India.
J Bacteriol. 2021 Jun 1;203(11). doi: 10.1128/JB.00582-20. Epub 2021 Mar 22.
Anthrax is a zoonotic disease caused by , a spore-forming pathogen that displays a chaining phenotype. It has been reported that the chaining phenotype acts as a virulence factor in In this study, we identify a serine/threonine protein kinase of , PrkC, the only kinase localized at the bacteria-host interface, as a determinant of chain length. , disruption strain (BAS Δ) grew as shorter chains throughout the bacterial growth cycle. A comparative analysis between the parent strain and BAS Δ indicated that the levels of proteins, BslO and Sap, associated with the regulation of the bacterial chain length, were upregulated in BAS Δ BslO is a septal murein hydrolase that catalyzes daughter cell separation and Sap is an S-layer structural protein required for the septal localization of BslO. PrkC disruption also has a significant effect on bacterial growth, cell wall thickness, and septa formation. Upregulation of in BAS Δ was also observed. Altogether, our results indicate that PrkC is required for maintaining optimum growth, cell wall homeostasis and most importantly - for the maintenance of the chaining phenotype.Chaining phenotype acts as a virulence factor in This is the first study that identifies a 'signal transduction protein' with an ability to regulate the chaining phenotype in We show that the disruption of the lone surface-localized serine/threonine protein kinase, PrkC, leads to the shortening of the bacterial chains. We report upregulation of the de-chaining proteins in the PrkC disruption strain. Apart from this, we also report for the first time that PrkC disruption results in an attenuated cell growth, a decrease in the cell wall thickness and aberrant cell septa formation during the logarithmic phase of growth - a growth phase where PrkC is expressed maximally.
炭疽是一种由形成芽孢的病原体引起的人畜共患病，该病原体表现出成链表型。据报道，成链表型在[具体细菌名称未给出]中作为一种毒力因子。在本研究中，我们鉴定出[具体细菌名称未给出]的一种丝氨酸/苏氨酸蛋白激酶PrkC，它是唯一位于细菌 - 宿主界面的激酶，是[细菌名称]链长度的决定因素。[具体细菌名称未给出]缺失菌株（BAS Δ）在整个细菌生长周期中形成较短的链。亲本菌株与BAS Δ之间的比较分析表明，与细菌链长度调节相关的蛋白质BslO和Sap的水平在BAS Δ中上调。BslO是一种隔膜胞壁质水解酶，催化子细胞分离，而Sap是BslO隔膜定位所需的S层结构蛋白。PrkC缺失对细菌生长、细胞壁厚度和隔膜形成也有显著影响。在BAS Δ中也观察到[具体物质未给出]的上调。总之，我们的结果表明，PrkC是维持最佳生长、细胞壁稳态以及最重要的——维持成链表型所必需的。成链表型在[具体细菌名称未给出]中作为一种毒力因子。这是第一项鉴定出具有调节[具体细菌名称未给出]成链表型能力的“信号转导蛋白”的研究。我们表明，唯一的表面定位丝氨酸/苏氨酸蛋白激酶PrkC的缺失导致细菌链缩短。我们报道了PrkC缺失菌株中解链蛋白的上调。除此之外，我们还首次报道PrkC缺失导致细胞生长减弱、细胞壁厚度减小以及在对数生长期异常的细胞隔膜形成——在这个生长阶段PrkC表达量最大。
