mRNA Degradation vs Translation

Proteome-wide alterations in Escherichia coli translation rates upon anaerobiosis 2010

Combined fractional diagonal chromatography – COFRADIC enriched azidohomoalanine (azhal) containing peptides using tris-(2-carboxy-ethyl)- phosphine (TCEP) to selectively modify peptides Developed a pulse labeling method using the methionine analogue azhal Tested after 10 minutes of anaerobiosis

Immediate and strong increase in synthesis rate of proteins involved in anaerobic respiration and fermentation. The synthesis rates of glycolytic enzymes and PTS proteins increased as well, suggesting that the increased flux through glycolysis is not exclusively the result of metabolic regulation, but also regulated at the protein level. Most of the proteins found to be down-regulated in synthesis were ribosomal proteins. It has been well documented that under conditions of energy deficiency synthesis of rRNA is decreased leading to translational feedback inhibition of ribosomal proteins synthesis These changes are induced by small regulatory RNAs that affect translation

Changes in the proteome can occur independently of mRNA degradation

Poly(A)-polymerase I links transcription with mRNA degradation via σ S proteolysis 2006

Figure 6. PAPI-mediated effect on σ S proteolysis. A. σ S is expressed under stressful conditions (stationary phase). PAPI reduces σ S proteolysis under stressful conditions as shown by the decreased σ S in the mutant without PAPI (two columns on the right of each graph and the right side of the blot)

Figure 8. Interplay among transcription, degradation and proteolysis machineries in the control of BolA and σ S BolA levels in the cell PAPI reduces proteolysis of σ S caused by RssB and ClpX and reduces mRNA degradation caused by various enzymes. The increased σ S levels induce the transcription and translation of various other proteins

mRNA degradation, proteolysis, and transcription work in concert to control subsequent gene expression and protein generation

Papers h.gov/pubmed/ h.gov/pubmed/ h.gov/pubmed/ h.gov/pubmed/