期刊
NUCLEIC ACIDS RESEARCH
卷 37, 期 9, 页码 3021-3031出版社
OXFORD UNIV PRESS
DOI: 10.1093/nar/gkp148
关键词
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资金
- Japan Society for the Promotion of Science (JSPS) [15370099, 17310113, 19657002]
- Ajinomoto CO., INC.
- Grants-in-Aid for Scientific Research [19657002, 15370099, 17310113] Funding Source: KAKEN
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 restrictionmodification gene complexes, such death is triggered by restriction endonucleases 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.
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