On Friday, 10 May at 10:15 Toomas Mets will defend his doctoral thsis "RNA fragmentation by MazF and MqsR toxins of Escherichia coli".
Senior Research Fellow, PhD Niilo Kaldalu
Professor, PhD Gerhart Wagner, Uppsala University, Sweden
Lives of bacteria are full of perils: they have to cope with dangerous chemicals, hostile neighbours and limited nutrients. To counter various hazards, bacteria have developed many stress response mechanisms. Bacterial toxin-antitoxin systems are small parasitic modules, which have been in some cases also adopted into stress response pathways. These genetic units encode for an autotoxic protein and an antitoxin that neutralizes the toxin. Antitoxins are labile and need to be constantly produced to inhibit the extremely stable toxins. Thus, when the module is lost or antitoxin production gets hindered the toxins become free to inhibit the growth. Toxins involved in stress response are mainly considered to be regulators of growth, which reduce the metabolic activity of cells in response to harmful conditions. Recently, some toxin-antitoxin systems have been reported to have a more sophisticated function: the regulation of specific genes. The most prominent example is the MazF toxin of Escherichia coli, which is an endoribonuclease hypothesized to reprogram the translational machinery during various stresses. It is speculated that MazF removes a piece of the 3’ end from 16S rRNA in mature ribosomes, which results in altered translational specificity. Such modified ribosomes are thought to translate stress-related transcripts with truncated 5’ UTR-s, which are hypothesized to also be generated by MazF. We studied the RNA cleavage by MazF and another endoribonuclease toxin, MqsR, in Escherichia coli and saw no evidence for such elaborate translational reprogramming. Instead, we show that MazF and MqsR act as growth inhibitors, which cleave unstructured RNA. Traditionally, endoribonuclease toxins of Escherichia coli are viewed only as degraders of mRNA, but our data implies that growth arrest is also facilitated through degradation of precursor rRNA.