yneA mRNA instability is involved in temporary inhibition of cell division during the SOS response of Bacillus megaterium.

The SOS response, a mechanism enabling bacteria to cope with DNA damage, is strictly regulated by the two major players, RecA and LexA (Bacillus homologue DinR). Genetic stress provokes formation of ssDNA-RecA nucleoprotein filaments, the coprotease activity of which mediates the autocatalytic cleavage of the transcriptional repressor DinR and ensures the expression of a set of din (damage-inducible) genes, which encode proteins that enhance repair capacity, accelerate mutagenesis rate and cause inhibition of cell division (ICD). In Bacillus subtilis, the transcriptional activation of the yneAB-ynzC operon is part of the SOS response, with YneA being responsible for the ICD. Pointing to its cellular function in Bacillus megaterium, overexpression of homologous YneA led to filamentous growth, while ICD was temporary during the SOS response. Genetic knockouts of the individual open reading frames of the yneAB-ynzC operon increased the mutagenic sensitivity, proving - for the first time in a Bacillus species - that each of the three genes is in fact instrumental in coping with genetic stress. Northern- and quantitative real-time PCR analyses revealed - in contrast to other din genes (exemplified for dinR, uvrBA) - transient mRNA-presence of the yneAB-ynzC operon irrespective of persisting SOS-inducing conditions. Promoter test assays and Northern analyses suggest that the decline of the ICD is at least partly due to yneAB-ynzC mRNA instability.