Gene Regulation III

In a diauxic shift of glucose and xylose, why is there another exponential and stationary phase after the initial one?

This is because bacteria can sense that there is no glucose but there is xylose present (can tell the difference between sugars). Therefore, it needs time to adapt and figure out how to grow since xylose is not preferential before it can grow exponentially again.

When glucose is low, what level if cAMP at?

Can be abundant

Is the lac operon subject to catabolite repression?

Yes

Where is the CAP binding site? What does it do?

It is next to the promotor and it recruits polymerase to the promotor for efficient transcription

Does CAP bind to DNA or RNA?

DNA

If there is glucose in the medium, do you need lacZ?

No you do so it is turned off when glucose is high (b-galactosidase breaks lactose into glucose and galactose)(when it is low then it can be turned on)

Is there negative control in the trp operon? What type of regulation is it?

Yes there is and allosteric regulation

What can the operator region of trp be bound by?

A repressor

When is the repressor able to bind to DNA?

When the repressor is bound to trp

Can RNA polymerase bind to the operator when there is an inactive repressor?

Yes

Why do we have negative regulation of the trp operon?

To not waste energy and resources

Can sigma 54 and RNA polymerase form an open complex on their own?

No

What does the sigma 54 and RNA polymerase complex need help from?

NtrC bound at enhancer sequences far upstream from the promotor (approximately 150 base pairs away from the start site)

If there is an extracellular signal sent, what does it need to do?

It needs help to get to the polymerase

Since NtrC is far away from the polymerase and sigma 54, how does it send the signal it receives?

The distance is made up by a conformation change in the DNA where it folds back in on itself (forms a loop)

If you damage NtrC or prevent DNA looping, what happens?

You will not get transcription of genes