Nucleic Acids Research Advance Access originally published online on March 20, 2009
Nucleic Acids Research 2009 37(9):3021-3031; doi:10.1093/nar/gkp148
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Nucleic Acids Research, 2009, Vol. 37, No. 9 3021-3031
© 2009 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Genomics |
From damaged genome to cell surface: transcriptome changes during bacterial cell death triggered by loss of a restriction–modification gene complex
1Ajinomoto CO., INC., 1-1 Suzuki-cho, Kawasaki-ku, Kawasaki-shi, Kanagawa 210-8681, 2Department of Medical Genome Sciences, Graduate School of Frontier Science, University of Tokyo, 3Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639 and 4Graduate Program in Biophysics and Biochemistry, Graduate School of Science, University of Tokyo, Japan
*To whom correspondence should be addressed. Email: youko_kuwabara{at}ajinomoto.com
Received December 29, 2008. Revised February 19, 2009. Accepted February 19, 2009.
Genetically programmed cell deaths play important roles in unicellular prokaryotes. In postsegregational killing, loss of a gene complex from a cell leads to its descendants’ deaths. With type II restriction–modification gene complexes, such death is triggered by restriction endonuclease's attacks on under-methylated chromosomes. Here, we examined how the Escherichia coli transcriptome changes after loss of PaeR7I gene complex. At earlier time points, activation of SOS genes and 
E-regulon was noticeable. With time, more SOS genes, stress-response genes (including S-regulon, osmotic-, oxidative- and periplasmic-stress genes), biofilm-related genes, and many hitherto uncharacterized genes were induced, and genes for energy metabolism, motility and outer membrane biogenesis were repressed. As expected from the activation of E-regulon, the death was accompanied by cell lysis and release of cellular proteins. Expression of several E-regulon genes indeed led to cell lysis. We hypothesize that some signal was transduced, among multiple genes involved, from the damaged genome to the cell surface and led to its disintegration. These results are discussed in comparison with other forms of programmed deaths in bacteria and eukaryotes.