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首页> 外文期刊>Journal of bacteriology >Isocitrate Lyase Supplies Precursors for Hydrogen Cyanide Production in a Cystic Fibrosis Isolate of Pseudomonas aeruginosa
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Isocitrate Lyase Supplies Precursors for Hydrogen Cyanide Production in a Cystic Fibrosis Isolate of Pseudomonas aeruginosa

机译：异柠檬酸裂合酶为铜绿假单胞菌的囊性纤维化分离物中的氰化氢生产提供前体

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Pseudomonas aeruginosa colonizes and can persist in the lungs of cystic fibrosis (CF) patients for decades. Adaptation of P. aeruginosa to the CF lung environment causes various genotypic and phenotypic alterations in the bacterium that facilitate persistence. We showed previously that isocitrate lyase (ICL) activity is constitutively upregulated in the P. aeruginosa CF isolate FRD1. We show here that high ICL activity in FRD1 contributes to increased hydrogen cyanide (HCN) production by this isolate. Disruption of aceA, which encodes ICL, results in reduced cyanide production by FRD1 but does not affect cyanide production in the wound isolate PAO1. Cyanide production is restored to the FRD1aceA mutant by addition of glyoxylate, a product of ICL activity, or glycine to the growth medium. Conversion of glyoxylate to glycine may provide a mechanism for increased cyanide production by P. aeruginosa growing on compounds that activate the glyoxylate pathway. Consistent with this hypothesis, disruption of PA5304, encoding a putative d-amino acid dehydrogenase (DadA), led to decreased cyanide production by FRD1. Cyanide production was restored to the FRD1dadA mutant by the addition of glycine, but not glyoxylate, to the growth medium, suggesting that loss of the ability to convert glyoxylate to glycine was associated with the dadA mutation. This was supported by increased glycine production from toluene-treated FRD1 cells with the addition of glyoxylate compared to FRD1dadA cells. This study indicates a larger role for ICL in the physiology and virulence of chronic isolates of P. aeruginosa than previously recognized.
机译：铜绿假单胞菌定居并可以在囊性纤维化（CF）患者的肺部持续存在数十年。 P的改编。 CF肺环境中的铜绿假单胞菌会导致细菌中各种基因型和表型改变，从而促进持久性。我们先前表明， P中异柠檬酸裂合酶（ICL）的活性是组成性上调的。铜绿CF分离株FRD1。我们在这里显示FRD1中的高ICL活性有助于通过这种分离物增加氰化氢（HCN）的产量。编码ICL的 aceA 的破坏导致FRD1减少氰化物的产生，但不影响伤口分离株PAO1中氰化物的产生。通过向生长培养基中添加乙醛酸盐（ICL活性的产物）或甘氨酸，可将氰化物的生成恢复为FRD1 aceA 突变体。乙醛酸酯向甘氨酸的转化可以提供一种通过 P增加氰化物产量的机制。铜绿假单胞菌生长在激活乙醛酸途径的化合物上。与此假设相一致，编码假定的d-氨基酸脱氢酶（DadA）的PA5304的破坏导致FRD1氰化物产量降低。通过向生长培养基中添加甘氨酸而不是乙醛酸，可将氰化物的产生恢复至FRD1 dadA 突变体，这表明乙醛酸转化为甘氨酸的能力丧失与 dadA相关突变。与FRD1 dadA 细胞相比，甲苯处理的FRD1细胞通过添加乙醛酸酯增加了甘氨酸的产量，从而支持了这一点。这项研究表明ICL在 P慢性分离株的生理和毒力中具有更大的作用。铜绿

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