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MxiJ是一种参与志贺氏菌Ipa侵袭素分泌的脂蛋白,与耶尔森氏菌Yop蛋白的分泌因子YscJ同源。

MxiJ, a lipoprotein involved in secretion of Shigella Ipa invasins, is homologous to YscJ, a secretion factor of the Yersinia Yop proteins.

作者信息

Allaoui A, Sansonetti P J, Parsot C

机构信息

Unité de Pathogénie Microbienne Moléculaire, Unité INSERM 199, Institut Pasteur, Paris, France.

出版信息

J Bacteriol. 1992 Dec;174(23):7661-9. doi: 10.1128/jb.174.23.7661-7669.1992.

DOI:10.1128/jb.174.23.7661-7669.1992
PMID:1332940
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC207479/
Abstract

Shigella flexneri causes bacillary dysentery by invading epithelial cells of the colonic mucosa. The invasion process requires the synthesis and secretion of the virulence plasmid-encoded Ipa proteins. Using TnphoA mutagenesis, we have identified two virulence plasmid genes, mxiJ and mxiM, that encode proteins exported by the general export pathway. Analysis of the MxiJ and MxiM deduced amino acid sequences suggested that mxiJ and mxiM might encode lipoproteins, which was confirmed by [3H]palmitate labeling of MxiJ:PhoA and MxiM:PhoA fusion proteins. A mxiJ mutant was unable to invade HeLa cells, to induce the formation of plaques on confluent monolayers of HeLa cells, and to provoke keratoconjunctivitis in guinea pigs. In addition, secretion of seven polypeptides, including IpaA, IpaB, and IpaC, was abolished in the mxiJ mutant. Sequence comparisons indicated that MxiJ and MxiH, which is encoded by a gene located upstream from mxiJ, are homologous to the Yersinia enterocolitica YscJ and YscF proteins, respectively.

摘要

福氏志贺菌通过侵入结肠黏膜上皮细胞引发细菌性痢疾。侵袭过程需要合成并分泌毒力质粒编码的Ipa蛋白。利用TnphoA诱变,我们鉴定出两个毒力质粒基因mxiJ和mxiM,它们编码由通用输出途径输出的蛋白。对MxiJ和MxiM推导的氨基酸序列分析表明,mxiJ和mxiM可能编码脂蛋白,这通过对MxiJ:PhoA和MxiM:PhoA融合蛋白进行[3H]棕榈酸酯标记得以证实。mxiJ突变体无法侵入HeLa细胞,无法在HeLa细胞汇合单层上诱导噬斑形成,也无法在豚鼠中引发角结膜炎。此外,mxiJ突变体中包括IpaA、IpaB和IpaC在内的七种多肽的分泌被消除。序列比较表明,MxiJ和由位于mxiJ上游的基因编码的MxiH分别与小肠结肠炎耶尔森菌的YscJ和YscF蛋白同源。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0435/207479/9dcc96b12b7c/jbacter00089-0184-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0435/207479/1ebf720ee955/jbacter00089-0183-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0435/207479/6f6cfe092842/jbacter00089-0183-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0435/207479/9dcc96b12b7c/jbacter00089-0184-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0435/207479/1ebf720ee955/jbacter00089-0183-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0435/207479/6f6cfe092842/jbacter00089-0183-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0435/207479/9dcc96b12b7c/jbacter00089-0184-a.jpg

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本文引用的文献

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Experimental keratoconjunctivitis shigellosa.实验性志贺菌性角膜结膜炎
Acta Microbiol Acad Sci Hung. 1957;4(4):367-76.
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Involvement of a plasmid in the invasive ability of Shigella flexneri.一种质粒与福氏志贺菌侵袭能力的关系。
[基因名称]基因的失活诱导生物膜形成并影响细菌致病性。 (这里原文中“the Gene of ”处基因名称缺失,需根据实际情况补充完整后翻译会更准确)
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