INTERNALIN-MEDIATED INVASION OF EPITHELIAL-CELLS BY LISTERIA-MONOCYTOGENES IS REGULATED BY THE BACTERIAL-GROWTH STATE, TEMPERATURE AND THE PLEIOTROPIC ACTIVATOR PRFA
INTERNALIN-MEDIATED INVASION OF EPITHELIAL-CELLS BY LISTERIA-MONOCYTOGENES IS REGULATED BY THE BACTERIAL-GROWTH STATE, TEMPERATURE AND THE PLEIOTROPIC ACTIVATOR PRFA
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DOI：
10.1111/j.1365-2958.1993.tb01223.x
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发表时间：
1993-09-01
影响因子：
3.6
通讯作者：
COSSART, P
中科院分区：
文献类型：
--
作者：
DRAMSI, S;KOCKS, C;COSSART, P
单核细胞增生李斯特菌进入上皮细胞需要inIA的表达，inIA是包含两个基因的操纵子的第一个基因：inIA，其编码内化蛋白，一种800个氨基酸的蛋白质，和inIB，其编码630个氨基酸的蛋白质。我们在这里报告，inI基因座转录的两个成绩单在恒定的相对比例：5 kb的成绩单跨越inIA和inIB，和2.9 kb的成绩单，仅涵盖inIA。该启动子位于距inIA的GTG起始子397 bp处，并且在其-35区域中显示与在由多效性激活剂prfA控制的启动子中发现的回文序列相似的回文序列。inI基因座的转录与其他几个L.单核细胞增多症毒力基因，由prfA激活并受温度调节-在37 ℃比25 ℃表达更高-和细菌生长状态。它在指数生长期间是最大的，并且与细菌在人上皮细胞系Caco-2中的最大侵袭力相关。它还与细菌表面上存在的最大量的内化相关。还在培养物上清液中检测到大量的内化素。两者合计，这些数据表明，表面结合的内化蛋白在细菌进入中起着重要作用，但不排除释放形式的作用。
Entry of Listeria monocytogenes into epithelial cells requires expression of inIA, the first gene of an operon comprising two genes: inIA, which encodes internalin, a 800-amino-acid protein, and inIB, which encodes a 630-amino-acid protein. We report here that the inI locus is transcribed on two transcripts in constant relative ratio: a 5 kb transcript spanning inIA and inIB, and a 2.9 kb transcript that covers only inIA. The promoter is located 397 bp from the GTG initiator of inIA and displays in its -35 region a palindrome similar to that found in promoters controlled by the pleiotropic activator prfA. Transcription of the inI locus is, as are several other L. monocytogenes virulence genes, activated by prfA and regulated by temperature- with higher expression at 37-degrees-C versus 25-degrees-C-and bacterial growth state. It is maximal during exponential growth and correlates with maximal invasivity of the bacteria in the human epithelial cell line Caco-2. It also correlates with maximum amounts of internalin present on the bacterial surface. Internalin is also detected in substantial amounts in culture supernatants. Taken together, these data suggest that surface-bound internalin plays an important role in bacterial entry but do not exclude a role for the released form.