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Initiation - Coggle Diagram

- - - - add lactose to analogue X-gal
      - this forms a blue product when lacZ is expressed
    - - negative mutants have never repressed operon so lacZ is always expressed
      - so normal lacL is a repressor
      - negative mutants are recessive, since functional lacL positive repressor can bind to DNA and restore regulation
      - lacLs
        
        super repressed mutant
        
        is dominant
        
        has no inducer binding sites so allolactose can never bind so repressor is always bound
    - - lacOc mutants never have a repressed operon, so lacZ is always expressed
      - lacOc is dominant
      - lacO only affects genes it binds to
  - - - inhibits adenyl cyclase so cAMP levels are low
      - cAMP binds to CAP (a protein) that bonds to the lac operon at the CAP site
      - glucose enters via protein IIC and is phosphorylated and associated with proteins IIA, IIB and HPr
      - Protein IIA becomes dephosphorylated when transported
      - phosphorylated form stimulates adenyl cyclase so no glucose transport means adenyl cyclase is inhibited
- - - - has attachment site sequence
      - requires integrase, which is coded by an early gene
      - integrase helps strands line up and causes a ds break
    - - when phage produces turbid plaques the host is not lysed
      - mutants of phage lambda had clear plaques so only lytic
      - mutants found to be mutants in 1 of 3 genes and called cI, cII, cIII
    - - N is an antiterminator, which allows cIII, xis and int to be transcribed
      - cI gene encodes for lambda repressor and its promoter is the promoter for repressor establishment (Pre)
      - Pre is activated by cII (cIII helps to stabilise cII, because it inhibits HflB which would otherwise attack cII, HflB is made when the cell is healthy and cIII is made when the cell is surrounded by other cells- it needs to justify making new phages)
      - lambda repressor inhibits both operons, so inhibits cII and cIII, so cI has another promoter- the promoter for repressor maintenance (Prm)
      - lambda promotes Prm and induces its expression to make more lambda so no lytic cycle
  - - - blocks the binding of lambda
      - also stops the production of cII
      - it interacts with lambda only on the right operator
    - - it has 3 operator regions (O3, O2, O1)
      - O1 overlaps with the rightward promoter, and O3 overlaps with Prm
      - lambda will always attempt to bind to O1, which blocks the rightward promoter to stop lytic cycle in low concentrations
      - lambda then binds to O2 which aids in the transcription of Prm, which then makes more lsmbda
      - if lambda is too high it binds to O3 which blocks Prm to reduce it concentration (autogenous control)
    - - CRO will always bind to O3 to limit lambda production
      - then bind to O2 then O1
      - binding to O1 inhibit rightward promoter and stops lytic transcription, but by the time the concentration gets high enough the lytic cycle is near completion
  - - - high levels promotes lysogeny by activating Pre and prevents Q (which is a late gene anti terminator , so S and R are not transcribed)
      - Q is not transcribed because a complementary RNA strand is transcribed and binds to Q so neither can be transcribed
      - it also activates a special promoter for integrase, so more integrase than exigase
    - - Under extreme stress the bacteria expresses RecA as an SOS response
      - RecA cuts the lambda repressor
      - so all genes are transcribed, but it does not go back into lysogeny because RecA will just cleave lambda repressor again
      - RecA is activated by ssDNA (which are produced during the stress)