The Bacteriophage Genetic Switch

[ennui]

The [math]\lambda[/math] bacteriophage has one of the most extensively studied 'molecular switches' in molecular genetics. The Cro/cI system appears to control the decision of the virus to go into a lytic or lysogenic cycle.

 

cI is mainly responsible for lysogeny, and Cro [+cII] for lysis. I know that the occupation of the rightward operator (O[math]_{}R[/math]) and its three binding sites (O[math]_{}R[/math]1,O[math]_{}R[/math]2,O[math]_{}R[/math]3) determine the repression of P[math]_{}R[/math] and P[math]_{}L[/math], and hence halt Cro expression. They form an octamer with the leftward operator and 'bend' the DNA.

 

But what is it in the bacterium that leads to a drop in cI levels, and hence a switch to the lytic stage? Some journals have hinted at cAMP levels affecting the transcription of cI, but I can't seem to find any detailed information about why the cI levels would drop and relax the repression of Cro transcription.

 

Does anyone know a journal which points this out? Or could anyone familiar with this bacteriophage help explain it? Much appreciated.

[CharonY]

Lambda (as well as a number of other phages) are basically using bacterial regulation to determine their own status. It is coupled to the SOS response of the cell (activation of RecA, autoproteolysis of LexA and so on). The reaction is analogous to the induced cleavage of LexA by RecA. CI has a slow self/cleavage that is a stabilized and promoted by the activated RecA. The CI cleavage is far slower, though.

 

This kind of information is easier found in textbooks as in journals as it has found its way into the realm of basic or common knowledge (and hence are rarely cited anymore).

[ennui]

Yeah it was hard to find in journals - even reviews. They were more occupied with explaining the mechanisms. But now I know everything I need to know - thanks!

[luminogenics]

Yeah this all happen when the host cell has been exposed to environmental stress. Including UV light and starvation. In either of these cases internal levels of the repressor drop and you get activation. All of these promoters are leaky anyway, what is important is the volume and redundancy of promoter sites. In this case only when the cell has been starving for a couple hours, and finds itself in a condition of excess waste it's not going to be able to keep up the level of protein production to keep the virus from escaping. Same for UV light, even if the cell is growing fine, if it finds itself replicating mutations the promoter and repressor sites are going to change and the repressor won't fit as well, and again the virus pops out.

 

I would suggest if you want to find a good article either look for a paper where they describe the structure of the repressor (Cell circa 2001) or, look back to the initial sequencing of the promoter region.

Edited April 26, 2009 by Sayonara³
I forgot something

[GDG]

You might find the Wiki article helpful.