revised 9 July 2003
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So, you might ask yourself, "how is it that glucose blocks the action of lactose, isn't this one of the original observations that we set out to explain?" You are of course right, we have not answered that question. A bacterium that spends energy building molecules it can get "for free" from its environment will be at a disadvantage compared to neighbors who exploit these molecules and used the energy saved for other tasks. On the other hand, if the environment changes, the ability to synthesize your own material provides a strong advantage. How do we resolve these conflicting strategies? It is common to find that parasitic organisms are simpler than free-living organisms. why might that be? (COMPLETE) |
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E. coli, and many other organisms, uses higher level regulatory schemes, known as "modulons" to adapt to global changes in its environment. There is a 'heat shock' modulons to protect cells from high temperatures. The lac operon is part of a larger regulon associated with metabolic processes. For example, when external glucose levels are high, the bacteria does not need to use alternative energy sources. It therefore represses the synthesis of many genes involved in using alternative energy sources. |
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A more detailed explanation (avoid it if you want).As external resources drop, the rate of intracellular ATP production also drops -- this sets off an alarm reaction - the activation of the phosphotransferase system (PTS). Activation of PTS leads to the phosphorylation and activation of the IIAglc protein (encoded by the catabolite repression resistance or crr) gene. Activated IIAglc activates the membrane-bound glucose transporter, so that the cell can capture as much of the glucose that remains in the environment as possible. Moreover, the unphosphorylated form of IIAglc acts to inhibit other permeases -- keeping possible inducers out of the cell. Activated IIAglc also activates the enzyme adenylate cyclase (AC - encoded by the cyaA gene). AC catalyze the reaction ATP to cAMP. cAMP is an alarmone, which activates the carbon starvation or carbon catabolyte repression modulon. cAMP binds to CRP (catabolyte repressor protein or crp - previously known as cAMP-binding protein or CAP in older literature). The cAMP-CRP complex binds to the promoters of the CCR modulon. The binding of the cAMP-CRP complex makes these operons regulateable by their specific inducers. In the case of the lac operon, if lactose is not present, there is only a slight increase in the basal transcription of the lac operon genes. If lactose is present, however, the operon is expressed at high levels. |
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Is the increased leakiness of the lac operon when the CCR modulon is activate beneficial to the cell, or just a molecular "mistake"? (COMPLETE) |
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revised 9 July 2003 |
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