SCAN:Studies on the post-transcriptional regulation of the small non-coding RNA MicA

ITQB- Scan Seminar

Title: Studies on the post-transcriptional regulation of the small non-coding RNA MicA

Speaker: Sandra Cristina Viegas

Affiliation: Post-Doc Fellow
Control of Gene Expression Laboratory

Abstract:

Eukaryotic and prokaryotic cells contain a wealth of small non-coding RNA molecules which control gene expression. The mechanisms by which sRNAs modulate gene expression are diverse; nonetheless, two general modes of action have been established, dividing regulatory RNAs into two main classes. They can modulate the activity of proteins or act by base pairing with one or more target messenger RNAs. The majority of the examples known belong to this second class, and directly bind to their specific target messenger RNA molecules to impair its translation and/or promote its degradation.
To understand the regulation by small RNAs it is fundamental to study their turnover since it can change their levels in the cell. MicA is a trans-encoded small non-coding RNA (encoded at a different genomic location of its mRNA target), conserved among many enterobacteria. MicA downregulates porin-expression in stationary-phase and its main targets in Salmonella are the outer membrane protein OmpA and the LamB maltoporin.
The work presented centers on the analysis of the expression profile of MicA in strains of Salmonella typhimurium mutant for ribonucleases. In particular, we have found that the fine-tuned regulation of MicA requires the action of two main endoribonucleases; while RNase E degrades isolated MicA molecules, RNase III degrades MicA bound to its target.  Proteins similar to RNase III are major actors in RNA regulation in eukaryotes. In a process known as RNA interference or gene silencing, small RNAs bind to the RNA of specific target genes, promoting their degradation and impeding the production of the respective protein. The fact that, in Salmonella, MicA is cleaved by RNase III in a target-dependent fashion, with the concomitant decay of the mRNA target, strengthens the RNase III role in the regulation of gene expression, also in bacteria.