Abstract
We report a novel post-transcriptional control of the ptsG gene encoding the major glucose transporter IICBGlc. We demonstrate that the level of IICBGlc is markedly reduced when the glycolytic pathway is blocked by a mutation in either the pgi or pfkA gene encoding phosphoglucose isomerase or phosphofructokinase, respectively. This down-regulation of ptsG is not exerted at the transcriptional level. Both northern blot and S1 analyses demonstrate that the mutation dramatically accelerates the degradation of ptsG mRNA. The degradation of ptsG mRNA occurs in wild-type cells when α-methylglucoside, a non-metabolizable analog of glucose, is present in the medium. The addition of any one of the glycolytic intermediates downstream of the block prevents the degradation of ptsG mRNA. The rapid degradation of ptsG mRNA is eliminated when RNase E is thermally inactivated. We conclude that the glycolytic pathway controls ptsG expression by modulating RNase E-mediated mRNA degradation. This is the first instance in which the glycolytic flux has been shown to affect the expression of a specific gene through mRNA stability.
Original language | English |
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Pages (from-to) | 3587-3595 |
Number of pages | 9 |
Journal | EMBO Journal |
Volume | 20 |
Issue number | 13 |
DOIs | |
Publication status | Published - 2001 Jul 2 |
Externally published | Yes |
Keywords
- Glucose transporter
- Glycolysis
- PTS
- RNase E
- mRNA degradation
ASJC Scopus subject areas
- Neuroscience(all)
- Molecular Biology
- Biochemistry, Genetics and Molecular Biology(all)
- Immunology and Microbiology(all)