Influence of Na+, dicarboxylic amino acids, and pH in modulating the low-calcium response of Yersinia pestis
Influence of Na+, dicarboxylic amino acids, and pH in modulating the low-calcium response of Yersinia pestis
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DOI：
10.1128/iai.73.8.4743-4752.2005
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发表时间：
2005-08-01
影响因子：
3.1
通讯作者：
Brubaker, RR
中科院分区：
文献类型：
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作者：
Brubaker, RR
耶尔森氏菌的毒力部分是通过共享的约70 kb质粒（鼠疫耶尔森氏菌的pCD和肠致病性假结核耶尔森氏菌和小肠结肠炎耶尔森氏菌的pYV）介导低钙反应而提升的。该表型的特点是在37℃下，通过表达pCD/ pyv编码的毒力效应物（Yops和LcrV）在Ca2+缺乏的培养基中抑菌，或通过>= 2.5 mM Ca2+ (Lcr(+))抑制Yops和LcrV的营养生长和抑制Yops和LcrV。Yops和LcrV的调控已被明确，但除了Na+ + l -谷氨酸促进鼠疫杆菌的迅速限制外，对抑菌作用知之甚少。如图所示，在这种情况下，l -天冬氨酸取代了l -谷氨酸，但只有Na+加剧了对Ca2+的营养需求。在中性至微碱性pH（7.0至8.0）的Ca2+缺乏培养基中，鼠疫杆菌（但不包括肠致病性耶尔森菌）的抑菌作用是突然的，尽管将pH增加到8.5或9.0，特别是添加Na+（但不添加l-谷氨酸），促进了全面生长。添加l -谷氨酸（而不是Na+）有利于在酸性pH（5.0至6.5）下的Ca2+独立生长。无论添加Na+或l -谷氨酸，Yops和LcrV都能在pH为6.5 ~ 9.0的Ca2+缺乏培养基中产生，但它们在碱性pH下的表达量很少。提供l -谷氨酸的鼠疫杆菌的静止Ca2+饥饿Lcr（+）细胞首先排出l -天冬氨酸，然后破坏l -天冬氨酸。这些发现表明，Yops和LcrV的表达是抑制Ca2+缺乏的耶尔森菌的必要条件，但不是充分条件，并表明突然限制耶尔森菌需要Na+和已知的缺乏天冬氨酸解氨酶。
The virulence of yersiniae is promoted in part by shared approximate to 70-kb plasmids (pCD in Yersinia pestis and pYV in enteropathogenic Yersinia pseudotuberculosis and Yersinia enterocolitica) that mediate a low-calcium response. This phenotype is characterized at 37 degrees C by either bacteriostasis in Ca2+-deficient medium with expression of pCD/pYV-encoded virulence effectors (Yops and LcrV) or vegetative growth and repression of Yops and LcrV with >= 2.5 mM Ca2+ (Lcr(+)). Regulation of Yops and LcrV is well defined but little is known about bacteriostasis other than that Na+ Plus L-glutamate promotes prompt restriction of Y. pestis. As shown here, L-aspartate substituted for L-glutamate in this context but only Na+ exacerbated the nutritional requirement for Ca2+. Bacteriostasis of Y. pestis (but not enteropathogenic yersiniae) was abrupt in Ca2+-deficient medium at neutral to slightly alkaline pH (7.0 to 8.0), although increasing the pH to 8.5 or 9.0, especially with added Na+ (but not L-glutamate), facilitated full-scale growth. Added L-glutamate (but not Na+) favored Ca2+- independent growth at acidic pH (5.0 to 6.5). Yops and LcrV were produced in Ca2+-deficient media at pH 6.5 to 9.0 regardless of the presence of added Na+ or L-glutamate, although their expression at alkaline pH was minimal. Resting Ca2+-starved Lcr(+) cells of Y. pestis supplied with L-glutamate first excreted and then destroyed L-aspartate. These findings indicate that expression of Yops and LcrV is necessary but not sufficient for bacteriostasis of Ca2+-starved yersiniae and suggest that abrupt restriction of Y. pestis requires Na+ and the known absence of aspartate ammonia-lyase in this species.