1887

Abstract

The antisense RNA ArrS is complementary to a sequence in the 5′ untranslated region of the T3 mRNA, the largest transcript of , which encodes a transcriptional activator of the glutamate-dependent acid resistance system in . Expression of is strongly induced during the stationary growth phase, particularly under acidic conditions, and transcription is dependent on σ and GadE. The aim of the present study was to clarify the role of ArrS in controlling expression by overexpressing in . The results showed a marked increase in the survival of -overexpressing cells at 2 h after a shift to pH 2.5. This was accompanied by increased expression of , and . The level of T3 mRNA decreased markedly in response to overexpression, and was accompanied by a marked increase in mRNA T2. T2 mRNA had a monophosphorylated 5′ terminus, which is usually found in cleaved mRNAs, and no T2 mRNA was observed in an RNase III-deficient cell strain. In addition, T2 mRNA was not generated by a P3-deleted translational fusion. These results suggest strongly that T2 mRNA is generated via the processing of T3 mRNA. Moreover, the T2 mRNA, which was abundant in -overexpressing cells, was more stable than T3 mRNA in non-overexpressing cells. These results suggest that overexpression of ArrS positively regulates expression in a post-transcriptional manner.

Funding
This study was supported by the:
  • Research Promotion Award of the Faculty of Health Sciences, Kyorin University, Japan
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2014-05-01
2024-04-20
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