A genetic selection reveals functional metastable structures embedded in a toxin-encoding mRNA.

Post-transcriptional regulation plays important roles to fine-tune gene expression in bacteria. In particular, regulation of type I toxin-antitoxin (TA) systems is achieved through sophisticated mechanisms involving toxin mRNA folding. Here, we set up a genetic approach to decipher the molecular underpinnings behind the regulation of a type I TA in .

FASTBAC-Seq: Functional Analysis of Toxin-Antitoxin Systems in Bacteria by Deep Sequencing.

As the number of bacterial genomes and transcriptomes increases, so does the number of newly identified toxin-antitoxin (TA) systems. However, their functional characterization remains challenging, often requiring the use of overexpression vectors that can lead to misinterpretations of in vivo results. To fill this gap, we developed a systematic approach called FASTBAC-Seq (Functional AnalysiS of Toxin-Antitoxin Systems in BACteria by Deep Sequencing).

Type I Toxin-Antitoxin Systems: Regulating Toxin Expression via Shine-Dalgarno Sequence Sequestration and Small RNA Binding.

Toxin-antitoxin (TA) systems are small genetic loci composed of two adjacent genes: a toxin and an antitoxin that prevents toxin action. Despite their wide distribution in bacterial genomes, the reasons for TA systems being on chromosomes remain enigmatic. In this review, we focus on type I TA systems, composed of a small antisense RNA that plays the role of an antitoxin to control the expression of its toxin counterpart.

A fungal pathogen secretes plant alkalinizing peptides to increase infection.

Plant infections caused by fungi are often associated with an increase in the pH of the surrounding host tissue(1). Extracellular alkalinization is thought to contribute to fungal pathogenesis, but the underlying mechanisms are poorly understood. Here, we show that the root-infecting fungus Fusarium oxysporum uses a functional homologue of the plant regulatory peptide RALF (rapid alkalinization factor)(2,3) to induce alkalinization and cause disease in plants.