SOS response
The SOS response is a technical term in biology for a response of prokaryotic cells to severe DNA damage and one of the cell's repair systems . Such damage is caused, for example, by ionizing radiation , heat or chemical substances that change DNA.
Badly damaged DNA cannot replicate properly and leads to the death of both daughter cells during the subsequent cell division. The SOS response is a program that enables the affected cell to repair the damaged DNA first and only then to continue the cell cycle .
First, the RecA protein is activated by single-stranded DNA (which almost always occurs with major DNA damage). RecA constantly "measures" the condition of the DNA in the cell. The activated RecA now in turn splits the LexA repressor. When intact, LexA binds to certain regions of the DNA and blocks the transcription of the SOS-specific genes. With the cleavage of LexA, the transcription of these genes is released and DNA repair is started. The activated genes include sfiA , which inhibits cell division and thus gives the cell time to repair. Furthermore, so-called uvr genes are transcribed, which code for DNA repair proteins such as the ABC exonuclease . In addition, the LexA repressor regulates its own transcription and that of RecA, which means that as soon as the damage in the DNA has been repaired and the concentration of activated RecA falls, LexA accumulates again in the cell and the system returns to its stable initial state .
The SOS response is a general bacteria-specific response to major DNA damage. In contrast to "normal" DNA repair processes, the repair in the SOS response is only imprecise, i.e. with a significantly increased error rate and thus leads to numerous mutations. Ionizing radiation and short-wave UV radiation are therefore also used for randomized mutagenesis .
If the bacterium is lysogenic , an SOS response leads to the multiplication and lysis of a virus integrated in the bacterial genome . For example, the bacterial genome may contain bacteriophage lambda DNA . The phage's own protein lambda cI repressor prevents the phage from multiplying and lysing. If an SOS response takes place in the bacterium, the RecA protein not only splits its substrate LexA, but also cI and thus initiates the lytic pathway of the lambda phage. The phage can leave the weakened host cell and does not have to perish with it.
Eukaryotes have a similar system, with the p53 protein playing a crucial role here . If the DNA damage in a eukaryotic cell is too great for a repair, apoptosis is initiated.
The SOS response was hypothesized by Miroslav Radman in 1970 (published in 1974) and later confirmed.
Individual evidence
- ↑ Gordienko I, Rupp WD: A specific 3 'exonuclease activity of UvrABC . In: The EMBO journal . 17, No. 2, January 1998, pp. 626-33. doi : 10.1093 / emboj / 17.2.626 . PMID 9430653 . PMC 1170412 (free full text).
literature
- Nelson, Cox: Lehninger Principles of Biochemistry . WH Freeman & Company 2004, ISBN 0-7167-4339-6