Extrinsic noise prevents the independent tuning of gene expression noise and protein mean abundance in bacteria.

It is generally accepted that prokaryotes can tune gene expression noise independently of protein mean abundance by varying the relative levels of transcription and translation. Here, we address this question quantitatively, using a custom-made library of 40 Bacillus subtilis strains expressing a fluorescent protein under the control of different transcription and translation control elements. We quantify noise and mean protein abundance by fluorescence microscopy and show that for most of the natural transcription range of B. subtilis, expression noise is equally sensitive to variations in the transcription or translation rate because of the prevalence of extrinsic noise. In agreement, analysis of whole-genome transcriptomic and proteomic datasets suggests that noise optimization through transcription and translation tuning during evolution may only occur in a regime of weak transcription. Therefore, independent control of mean abundance and noise can rarely be achieved, which has strong implications for both genome evolution and biological engineering.

Specific accumulation of CYP94A1 transcripts after exposure to gaseous benzaldehyde: induction of lauric acid ω-hydroxylase activity in Vicia sativa exposed to atmospheric pollutants.

The effects of air pollutants such as aldehydes, ozone, nitrogen dioxide and benzene on fatty acid ω-hydroxylase activity in Vicia sativa microsomes have been investigated. Four days old etiolated V. sativa seedlings were exposed to different concentrations of selected pollutants for varying exposure times. Growing etiolated V. sativa seedlings in air containing the gaseous benzaldehyde (150 nM) led to an 8-fold enhancement of lauric acid ω-hydroxylase activity in microsomes of treated plants compared to controls grown in pure air (96 ± 10 versus 12 ± 2 pmol/min/mg protein, respectively). The induction increased with increasing gas phase concentrations (10-1300 nM) and the maximum of activity was measured after 48 h of exposure. Northern blot analysis revealed that this induction occurred via transcriptional activation of the gene coding for CYP94A1. The absence of CYP94A2 and CYP94A3 transcription activation together with the missing effect on epoxide hydrolases activities indicate the specificity of CYP94A1 induction by benzaldehyde. Exposure to nitrogen dioxide, ozone and formaldehyde also stimulated lauric acid ω-hydroxylases activity while exposure to benzene did not show any effect.