Positive correlation between tyrosine phosphorylation of CpsD and capsular polysaccharide production in Streptococcus pneumoniae
Positive correlation between tyrosine phosphorylation of CpsD and capsular polysaccharide production in Streptococcus pneumoniae
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DOI：
10.1128/jb.185.20.6057-6066.2003
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发表时间：
2003-10-01
影响因子：
3.2
通讯作者：
Yother, J
中科院分区：
文献类型：
--
作者：
Bender, MH;Cartee, RT;Yother, J
CPSA、CpsB、CPSC和CPSD是酪氨酸磷酸化调节系统的一部分，参与调节肺炎链球菌和许多其他革兰氏阳性和革兰氏阴性细菌的包膜合成。利用免疫印迹技术，我们观察到不同血清型肺炎链球菌荚膜多糖的不同梯形，发现聚合物从膜到细胞壁的转移与大小无关。在血清2型菌株D39中，cps2A、cps2B、cps2C或cps2D的缺失并不影响将囊膜转移到细胞壁的能力。Eps2C或cps2D的缺失导致只产生短链聚合物，而eps2C或cps2D编码自磷酸化酪氨酸激酶的两个结构域。Cps2A的功能尚不清楚，缺失突变体的聚合物梯形图谱与亲本相似，但被膜总量减少。酪氨酸磷酸酶和激酶抑制剂Cps2B的缺失导致包膜数量增加和正常的梯形图谱。然而，Cps2B突变体在静脉接种小鼠后显示出降低的毒力，并且不能在鼻咽定植，这表明对这些环境的感知或反应能力减弱。在D39及其等基因突变体中，被膜蛋白和酪氨酸磷酸化的Cps2D(Cps2D相似TOP)的数量直接相关。相反，在RX1(一种实验室传代的含有多种未知突变的D39衍生物)中，恢复2型胶囊的生产并删除cps2B会导致胶囊数量减少，但Cps2D类似的最高水平没有变化。因此，在RX1背景中缺失或缺陷的包膜外的一个因子在包膜合成的控制中是重要的。
CpsA, CpsB, CpsC, and CpsD are part of a tyrosine phosphorylation regulatory system involved in modulation of capsule synthesis in Streptococcus pneumoniae and many other gram-positive and gram-negative bacteria. Using an immunoblotting technique, we observed distinct laddering patterns of S. pneumoniae capsular polysaccharides of various serotypes and found that transfer of the polymer from the membrane to the cell wall was independent of size. Deletion of cps2A, cps2B, cps2C, or cps2D in the serotype 2 strain D39 did not affect the ability to transfer capsule to the cell wall. Deletion of eps2C or cps2D, which encode two domains of an autophosphorylating tyrosine kinase, resulted in the production of only short-chain polymers. The function of Cps2A is unknown, and the polymer laddering pattern of the cps2A deletion mutants appeared similar to that of the parent, although the total amount of capsule was decreased. Loss of Cps2B, a tyrosine phosphatase and a kinase inhibitor, resulted in an increase in capsule amount and a normal ladder pattern. However, Cps2B mutants exhibited reduced virulence following intravenous inoculation of mice and were unable to colonize the nasopharynx, suggesting a diminished capacity to sense or respond to these environments. In D39 and its isogenic mutants, the amounts of capsule and tyrosine-phosphorylated Cps2D (Cps2Dsimilar toP) correlated directly. In contrast, restoration of type 2 capsule production followed by deletion of cps2B in Rx1, a laboratory passaged D39 derivative containing multiple uncharacterized mutations, resulted in decreased capsule amounts but no alteration in Cps2Dsimilar toP levels. Thus, a factor outside the capsule locus, which is either missing or defective in the Rx1 background, is important in the control of capsule synthesis.