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首页> 外文期刊>Infection and immunity >GapA and CrmA Coexpression Is Essential for Mycoplasma gallisepticum Cytadherence and Virulence
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GapA and CrmA Coexpression Is Essential for Mycoplasma gallisepticum Cytadherence and Virulence

机译：GapA和CrmA共表达对于鸡支原体细胞黏附和毒力至关重要

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It was previously demonstrated that avirulent Mycoplasma gallisepticum strain Rhigh (passage 164) is lacking three proteins that are expressed in its virulent progenitor, strain Rlow (passage 15). These proteins were identified as the cytadhesin molecule GapA, the putative cytadhesin-related molecule CrmA, and a component of a high-affinity transporter system, HatA. Complementation of Rhigh with wild-type gapA restored expression in the transformant (GT5) but did not restore the cytadherence phenotype and maintained avirulence in chickens. These results suggested that CrmA might play an essential role in the M. gallisepticum cytadherence process. CrmA is encoded by the second gene in the gapA operon and shares significant sequence homology to the ORF6 gene of Mycoplasma pneumoniae, which has been shown to play an accessory role in the cytadherence process. Complementation of Rhigh with wild-type crmA resulted in the transformant (SDCA) that lacked the cytadherence and virulence phenotype comparable to that found in Rhigh and GT5. In contrast, complementation of Rhigh with the entire wild-type gapA operon resulted in the transformant (GCA1) that restored cytadherence to the level found in wild-type Rlow. In vivo pathogenesis trials revealed that GCA1 had regained virulence, causing airsacculitis in chickens. These results demonstrate that both GapA and CrmA are required for M. gallisepticum cytadherence and pathogenesis.
机译：先前已证明无毒的鸡支原体毒株R high （第164代）缺少在其有力祖细胞R low （段落15）。这些蛋白被鉴定为细胞粘附素分子GapA，推测的细胞粘附素相关分子CrmA，以及高亲和力转运蛋白系统HatA的组成部分。 R high 与野生型 gapA 的互补在转化子（GT5）中恢复了表达，但没有恢复细胞粘附性表型，并保持了鸡的无毒力。这些结果表明，CrmA可能在 M中起重要作用。鸡败血性细胞粘附过程。 CrmA由 gapA 操纵子中的第二个基因编码，并且与肺炎支原体的 ORF6 基因具有显着的序列同源性，这表明在细胞粘附过程中起辅助作用。 R high 与野生型 crmA 的互补导致转化子（SDCA）缺乏与R high 和GT5。相反，R high 与整个野生型 gapA 操纵子的互补导致转化子（GCA1）将细胞粘附力恢复到野生型R 低。体内发病机理试验表明，GCA1已恢复毒力，在鸡中引起气囊炎。这些结果表明， M同时需要GapA和CrmA。鸡败血性细胞粘附和发病机理。

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