dc.contributor.author |
Zhang, Y. |
|
dc.contributor.author |
Yan, D |
|
dc.contributor.author |
Xia, L. |
|
dc.contributor.author |
Zhao, X. |
|
dc.contributor.author |
Osei-Adjei, G. |
|
dc.contributor.author |
Xu, S. |
|
dc.contributor.author |
Huang, X. |
|
dc.date.accessioned |
2022-09-08T10:20:33Z |
|
dc.date.available |
2022-09-08T10:20:33Z |
|
dc.date.issued |
2017 |
|
dc.identifier.other |
10.1139/cjm-2016-0490 |
|
dc.identifier.uri |
http://atuspace.atu.edu.gh:8080/handle/123456789/218 |
|
dc.description.abstract |
Bacterial noncoding RNAs (ncRNA) regulate diverse cellular processes, including virulence and environmental fitness. The malS 5' untranslated region (named malS-5'UTR) was identified as a regulatory ncRNA that increases the invasive capacity of Salmonella enterica serovar Typhi. An IntaRNA search suggested base pairing between malS-5'UTR and hisG mRNA, a key gene in the histidine biosynthetic pathway. Overexpression of malS-5'UTR markedly reduced bacterial growth in minimal medium without histidine. Overexpression of malS-5'UTR increased mRNA from his operon genes, independently of the bax gene, and decreased HisG protein in Salmonella Typhi. RNA structure analysis showed base pairing of the malS-5'UTR RNA with the hisG mRNA across the ribosome binding site. Thus, we propose that malS-5'UTR inhibited hisG translation, probably by base pairing to the Shine-Dalgarno sequence. |
en_US |
dc.language.iso |
en |
en_US |
dc.publisher |
PubMed |
en_US |
dc.relation.ispartofseries |
vol;63 |
|
dc.subject |
ARNnc |
en_US |
dc.subject |
Salmonella enterica serovar Typhi |
en_US |
dc.subject |
Salmonella enterica sérovar Typhi |
en_US |
dc.subject |
hisG |
en_US |
dc.subject |
histidine |
en_US |
dc.subject |
malS-5′UTR |
en_US |
dc.subject |
ncRNA |
en_US |
dc.title |
The malS-5′ UTR regulates hisG, a key gene in the histidine biosynthetic pathway in Salmonella enterica serovar Typhi. |
en_US |
dc.type |
Article |
en_US |