DNA repair in Mycoplasma gallisepticum
- Equal contributors
1 Research Institute of Physico-Chemical Medicine, Malaya Pirogovskaya 1a, Moscow 119992, Russian Federation
2 Institute for Information Transmission Problems of the Russian Academy of Sciences, Bolshoy Karetny 19, Moscow 127994, Russian Federation
3 Moscow Institute of Physics and Technology, Institutsky 9, Dolgoprudny 141700, Russian Federation
4 Shemyakin–Ovchinnikov Institute of Bioorganic Chemistry of the Russian Academy of Sciences, Miklukho-Maklaya 16/10, Moscow 117997, Russian Federation
BMC Genomics 2013, 14:726 doi:10.1186/1471-2164-14-726Published: 23 October 2013
DNA repair is essential for the maintenance of genome stability in all living beings. Genome size as well as the repertoire and abundance of DNA repair components may vary among prokaryotic species. The bacteria of the Mollicutes class feature a small genome size, absence of a cell wall, and a parasitic lifestyle. A small number of genes make Mollicutes a good model for a “minimal cell” concept.
In this work we studied the DNA repair system of Mycoplasma gallisepticum on genomic, transcriptional, and proteomic levels. We detected 18 out of 22 members of the DNA repair system on a protein level. We found that abundance of the respective mRNAs is less than one per cell. We studied transcriptional response of DNA repair genes of M. gallisepticum at stress conditions including heat, osmotic, peroxide stresses, tetracycline and ciprofloxacin treatment, stationary phase and heat stress in stationary phase.
Based on comparative genomic study, we determined that the DNA repair system M. gallisepticum includes a sufficient set of proteins to provide a cell with functional nucleotide and base excision repair and mismatch repair. We identified SOS-response in M. gallisepticum on ciprofloxacin, which is a known SOS-inducer, tetracycline and heat stress in the absence of established regulators. Heat stress was found to be the strongest SOS-inducer. We found that upon transition to stationary phase of culture growth transcription of DNA repair genes decreases dramatically. Heat stress does not induce SOS-response in a stationary phase.