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牙龈卟啉单胞菌中蛋白酶表达的调控

Regulation of protease expression in Porphyromonas gingivalis.

作者信息

Tokuda M, Chen W, Karunakaran T, Kuramitsu H K

机构信息

Department of Oral Biology, State University of New York, Buffalo, New York 14214, USA.

出版信息

Infect Immun. 1998 Nov;66(11):5232-7. doi: 10.1128/IAI.66.11.5232-5237.1998.

Abstract

Although the strong protease activity of Porphyromonas gingivalis appears to be an important virulence property of these organisms, little information is currently available regarding the regulation of expression of the multiple protease genes. Utilizing the lacZ reporter gene strategy, the environmental factors which regulate the expression of the Arg-gingipain gene rgpA and the prtT protease gene were investigated. These two genes are reciprocally regulated since factors which retarded growth (iron depletion and nutrient limitation) appeared to upregulate rgpA expression while down-regulating prtT expression. However, inactivation of the major rgpA gene resulted in increased transcription of the prtT and tpr protease genes while decreasing expression of the Lys-gingipain kgp gene as detected by Northern blot analysis. By contrast, inactivation of the prtT gene did not significantly affect kgp expression but moderately decreased rgpA mRNA levels. These results indicate that the protease genes of P. gingivalis are not coordinately regulated and suggest that some of these enzymes play specific roles in the physiology and/or virulence of these organisms.

摘要

尽管牙龈卟啉单胞菌强大的蛋白酶活性似乎是这些微生物的一项重要毒力特性,但目前关于多个蛋白酶基因表达调控的信息还很少。利用lacZ报告基因策略,研究了调控精氨酸牙龈蛋白酶基因rgpA和prtT蛋白酶基因表达的环境因素。这两个基因受到相互调控,因为阻碍生长的因素(铁缺乏和营养限制)似乎上调rgpA的表达,而下调prtT的表达。然而,通过Northern印迹分析检测到,主要的rgpA基因失活导致prtT和tpr蛋白酶基因的转录增加,同时降低了赖氨酸牙龈蛋白酶kgp基因的表达。相比之下,prtT基因失活对kgp表达没有显著影响,但适度降低了rgpA的mRNA水平。这些结果表明,牙龈卟啉单胞菌的蛋白酶基因并非协同调控,提示其中一些酶在这些微生物的生理和/或毒力中发挥特定作用。

相似文献

1
Regulation of protease expression in Porphyromonas gingivalis.牙龈卟啉单胞菌中蛋白酶表达的调控
Infect Immun. 1998 Nov;66(11):5232-7. doi: 10.1128/IAI.66.11.5232-5237.1998.

引用本文的文献

本文引用的文献

1
Proteases of Porphyromonas gingivalis: what don't they do?牙龈卟啉单胞菌的蛋白酶:它们无所不能?
Oral Microbiol Immunol. 1998 Oct;13(5):263-70. doi: 10.1111/j.1399-302x.1998.tb00706.x.
2
Microbial etiological agents of destructive periodontal diseases.破坏性牙周疾病的微生物病原体。
Periodontol 2000. 1994 Jun;5:78-111. doi: 10.1111/j.1600-0757.1994.tb00020.x.

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