Identification and characterization of VapBC toxin–antitoxin system in Bosea sp. PAMC 26642 isolated from Arctic lichens

Abstract

Toxin-antitoxin (TA) systems are genetic modules composed of a toxin interfering with cellular processes and its cognate antitoxin, which counteracts the activity of the toxin. TA modules are widespread in bacterial and archaeal genomes. It has been suggested that TA modules participate in the adaptation of prokaryotes to unfavorable conditions. The Bosea sp. PAMC 26642 used in this study was isolated from the Arctic lichen Stereocaulon sp.. There are twelve putative type II TA loci in the genome of Bosea sp. PAMC 26642. Of these, nine functional TA systems have been shown to be toxic in Escherichia coli. The toxin inhibits growth, but this inhibition is reversed when the cognate antitoxin genes are co-expressed, indicating that these putative TA loci were bona fide TA modules. Only the BoVapC (AXW83_01405) toxin, a homolog of VapC, showed growth inhibition specific to low temperatures, which was recovered by the co-expression of BoVapB (AXW83_01400). Microscopic observation and growth monitoring revealed that the BoVapC toxin had bacteriostatic effects on the growth of E. coli and induced morphological changes. Quantitative real time polymerase chain reaction and northern blotting analyses showed that the BoVapC toxin had a ribonuclease activity on the initiator tRNAfMet, implying that degradation of tRNAfMet might trigger growth arrest in E. coli. This is the first study to identify the function of TA systems in an Arctic bacterium.

VapC10 toxin of the legume symbiont Sinorhizobium meliloti targets tRNASer and controls intracellular lifestyle

“…To date, most of the characterized VapC toxins target the initiator tRNA, tRNA fMet , as demonstrated for VapCs of S. flexneri , Leptospira interrogans [ 52 ], H. influenzae , S. Typhimurium, Bosea sp. [ 53 ], and for VapC2 and VapC21 of M. tuberculosis [ 54 ]. In addition, some VapCs in M. tuberculosis were shown to target elongator tRNA Gln(CUG) and tRNA Leu(CAG) (VapC11 [ 55 ]), tRNA Cys (VapC4 [ 56 ]), tRNA Trp(CCA) , and tRNA Ser(UGA and CGA) [ 52 ].…”

Bacterial Toxin-Antitoxin Systems’ Cross-Interactions—Implications for Practical Use in Medicine and Biotechnology

“…For instance, the pemIK modules were able to maintain plasmids in various strains of both E. coli and K. pneumoniae , whereas the ccdAB cassettes demonstrated higher specificity towards their own host strain [ 191 ]. Moreover, some TA toxins cause the host death upon loss of the plasmid, whereas some only hinder bacterial culture growth, acting as bacteriostatic agents, as was shown for the Hok and VapC toxins, respectively [ 192 , 193 ]. However, this effect probably mainly depends on the toxin concentration within the cell and on the timing of toxin induction under experimental conditions.…”