Abstract
Post-transcriptional regulation plays important roles to fine-tune gene expression in bacteria. In particular, regulation of type I toxin-antitoxin (TA) systems is achieved through sophisticated mechanisms involving toxin mRNA folding. Here, we set up a genetic approach to decipher the molecular underpinnings behind the regulation of a type I TA in Helicobacter pylori. We used the lethality induced by chromosomal inactivation of the antitoxin to select mutations that suppress toxicity. We found that single point mutations are sufficient to allow cell survival. Mutations located either in the 5' untranslated region or within the open reading frame of the toxin hamper its translation by stabilizing stem-loop structures that sequester the Shine-Dalgarno sequence. We propose that these short hairpins correspond to metastable structures that are transiently formed during transcription to avoid premature toxin expression. This work uncovers the co-transcriptional inhibition of translation as an additional layer of TA regulation in bacteria.
| Item Type: | Journal article |
|---|---|
| Faculties: | Biology > Department Biology I |
| Subjects: | 500 Science > 570 Life sciences; biology |
| URN: | urn:nbn:de:bvb:19-epub-83711-4 |
| ISSN: | 2050-084X |
| Language: | English |
| Item ID: | 83711 |
| Date Deposited: | 15. Dec 2021, 15:09 |
| Last Modified: | 27. Jan 2023, 08:19 |
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