The term “lysogenic” implies that prophages are capable of giving rise to active phages that lyse their host cells.
This occurs when the viral genome exits the bacterial chromosome and initiates
the lytic cycle. The triggers for this switch-over are usually
environmental factors such as mutagens (e.g. radiation and presence of certain
chemicals)
It depends on a few factors, such as how many phages
infected the cell, whether or not the cell is in good growth conditions, and so
on.
If the cell is in stress or has low amounts of
nutrients, the lysogenic pathway is typically activated.
The underlying mechanism has to do with a protein
cascade involving either the cro or cI protein that is encoded by the virus.
The cI protein is a repressor, and it will prevent the lytic genes from being
transcribed. By default the virus will transcribe the lytic genes, so they must
be repressed for lysogeny to occur.
Similarly, cro is also a
transcriptional repressor.
The two proteins
work in opposition to each other. cro binds to an operator, oR3, that is involved in
repressing cI, which may prevent cI from being expressed and thus preventing it from
repressing lytic genes (however the importance of this is debatable
because if you replace oR3, the cell can apparently still lyse).
There are numerous
other proteins, such as N and Q, that are involved. The N protein has to be
transcribed by the polymerase ‘anti-terminating’, or reading through a
termination signal. This will happen more frequently when the protein RNase III is present at
high concentrations.
The N protein is a lytic regulator. Thus,
when there are high amounts of RNase III there will be more N expressed which leads to the lytic cycle. RNase III is not a viral
protein. It is a host protein and the host expresses more of it when nutrients
are abundant. This is how the virus is able to ‘sense’ if nutrients are high
enough to enter the lytic cycle.