High concentrations of intracellular Ap4A and/or Ap5A in developing Myxococcus xanthus cells inhibit sporulation
High concentrations of intracellular Ap4A and/or Ap5A in developing Myxococcus xanthus cells inhibit sporulation
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正在发育的黄色粘球菌细胞中高浓度的细胞内 Ap4A 和/或 Ap5A 抑制孢子形成
作者：
Kimura;Y.;Tanaka;C.;Sasaki;K.;and Sasaki;M.
多磷酸二腺苷 (ApnA) 被认为是调节原核生物应激反应和生物膜形成的信号分子。然而，ApnA 在黄色粘球菌中的功能仍然未知。在这里，我们研究了 ApnA 在 M 中的作用。 xanthus，使用暴露于各种胁迫条件的野生型和 ApnA 水解酶 (apaH) 突变株。在饥饿培养基（CF琼脂）上培养的野生型andapaH突变细胞中，细胞内四磷酸二腺苷（Ap4A）和五磷酸二腺苷（Ap5A）的水平在发育的前16小时期间增加了几倍，然后逐渐下降。 16小时时，theapaH突变体中的Ap4A和Ap5A水平分别比野生型菌株高约5倍和11倍。野生型菌株的ApnA水解酶活性在发育的前8小时内增加了1.5倍，然后逐渐下降。 TheapaH突变体在野生型菌株形成孢子后1-2天形成孢子，接种到CF琼脂上5天后，活孢子产量是野生型菌株的5.5%。这些结果表明细胞内高水平的Ap4A和/或Ap5A可能抑制M。黄花孢子在发育早期阶段形成，细菌通过 ApnA 水解酶活性减少细胞内 Ap4A 和 Ap5A 的积累。
Diadenosine polyphosphates (ApnA) are thought to act as signalling molecules regulating stress responses and biofilm formation in prokaryotes. However, ApnA function inMyxococcus xanthusremains unknown. Here, we investigated the role of ApnA inM. xanthus, using the wild-type and ApnA hydrolase (apaH) mutant strains exposed to various stress conditions. In both wild-type andapaHmutant cells cultured on starvation medium (CF agar), the levels of intracellular diadenosine tetraphosphate (Ap4A) and pentaphosphate (Ap5A) increased several fold during the first 16 h of development and decreased gradually thereafter. The levels of Ap4A and Ap5A in theapaHmutant were about 5- and 11-fold higher than those in the wild-type strain at 16 h, respectively. ApnA hydrolase activity of the wild-type strain increased 1.5-fold during the first 8 h of development, and it then gradually decreased. TheapaHmutant formed spores 1–2 days after the wild-type strain did, and the yield of viable spores was 5.5 % of that in the wild-type strain 5 days after inoculation onto CF agar. These results suggest the possibility that high intracellular levels of Ap4A and/or Ap5A may inhibitM. xanthussporulation at the early stage of development and that the bacteria reduce intracellular Ap4A and Ap5A accumulation through ApnA hydrolase activity.