Enhanced synthesis of internalin A in aro mutants of Listeria monocytogenes indicates posttranscriptional control of the inlAB mRNA
Enhanced synthesis of internalin A in aro mutants of Listeria monocytogenes indicates posttranscriptional control of the inlAB mRNA
复制标题
DOI：
10.1128/jb.187.8.2836-2845.2005
复制
发表时间：
2005-04-01
影响因子：
3.2
通讯作者：
Goebel, W
中科院分区：
文献类型：
--
作者：
Stritzker, J;Schoen, C;Goebel, W
具有 aroA、aroB 或 aroE 缺失的单核细胞增多性李斯特菌突变体表现出内化素 A (InIA) 和 InIB 合成的强烈转录后上调，导致与野生型菌株相比，上皮 Caco-2 细胞的 InlA 介导的内化增加了 10 倍以上，微血管内皮细胞（人脑微血管内皮细胞）的 InIB 介导的内化增加了 4 倍以上。 InlA和InlB产量的增加不是由于PrfA和/或σ因子B (SigB)依赖性inlAB转录的增强，而是由于aro突变体中inLAB转录物的翻译增强引起的。所有 inLA(B) 转录物都有一个 396 个核苷酸的上游 5' 非翻译区 (UTR)。该 UTR 中引入的不同缺失导致 InlA 和 InlB 合成显着减少；然而，仍然观察到 aro 突变体中所有截短转录本的翻译增强。因此，inlAB转录物的翻译受到两种转录后控制模式的影响，一种由UTR结构介导，另一种由aro突变介导。后一种控制模式似乎与 aro 突变体的主要厌氧代谢有关。
Listeria monocytogenes mutants with deletions in aroA, aroB, or aroE exhibited strong posttranscriptional upregulation of internalin A (InIA) and InIB synthesis, which resulted in a more-than-10-fold increase in InlA-mediated internalization by epithelial Caco-2 cells and a 4-fold increase in InIB-mediated internalization by microvascular endothelial cells (human brain microvascular endothelial cells) compared to the wild-type strain. The increase in InlA and InlB production was not due to enhanced PrfA- and/or sigma factor B (SigB)-dependent inlAB transcription but was caused by enhanced translation of the inLAB transcripts in the aro mutants. All inLA(B) transcripts had a 396-nucleotide upstream 5' untranslated region (UTR). Different deletions introduced into this UTR led to significant reductions in InlA and InlB synthesis; enhanced translation of all of the truncated transcripts in the aro mutants was, however, still observed. Thus, translation of the inlAB transcripts was subject to two modes of posttranscriptional control, one mediated by the UTR structure and the other mediated by the aro mutation. The latter mode of control seemed to be related to the predominantly anaerobic metabolism of the aro mutants.