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18 Feb 2018

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1. If a bacterium with a wildtype lac operon is grown in the presence of lactose, high levels of transcription result for a while, however, eventually transcription is again down-regulated. If, on the other hand, the sugar IPTG is present (instead of lactose), transcription levels are high and remain high. What function do IPTG and lactose share? How are they differently affected by the operon product?

Lactose and IPTG are both inducers of the Lac-Operon. Lactose is a substance that the enzyme will react with (substrate), which is split or cleaved by the Beta-galactosidase. When you add lactose expressions level of lac operon will increase but as lactose is used by the beta-galactosidase expression levels of lac operon will decrease.

IPTG is a chemical cannot be split or cleaved by beta-galactosidase. The expression level of lac operon will remain the same.

Or Lactose can be easily broken down but IPTG cannot be broken down. What does expressions level mean?

2. If a lacI - bacterium is grown in the presence of the sugar X-gal, a blue dye appears; however, the concentration of X-gal decreases over time. What has happened to the X-gal?


If a lacI - bacterium is grown in the presence of the sugar X-gal, the Lacl is mutant or the gene is damaged which alters the genetic message carried by that gene. The LacI gene produces the repressor protein which switches off the operon, but since it is damaged no repressor protein is produced and the operon is switched on. The Lacl is transcribed into beta-galactosidase (lactose) The enzyme beta-galactosidase (lactose) splits or separates the X-gal which will result in decreased concentration of X-gal with time.

3. If a wildtype bacterium is grown in the presence of the sugar X-gal, transcription of the polycistronic m-RNA does not occur. What is X-gal unable to do? Without adding lactose (or genetically modifying the bacteria), how could you fix this problem

X-gal cannot form lactose, the repressor remains off and beta-galactosidase is not formed. This can be fixed by adding IPTG which can switch on the operon

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Elin Hessel
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19 Feb 2018

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Related questions

1) In the wildtype (the DNA sequence most commonly found in nature) lac operon, transcription is severely down-regulated. A mutation in lacI that causes an early stop codon in the sequence (called a lacI - strain) results in an operon that has high levels of transcription of the polycistronic m-RNA. What type of regulatory protein is the LacI protein (hint: we covered this type of protein in lecture)?

The Lac regulatory protein is called a repressor. (is this correct)

2) If a bacterium with a wildtype lac operon is grown in the presence of lactose, high levels of transcription result for a while, however, eventually transcription is again down-regulated. If, on the other hand, the sugar IPTG is present (instead of lactose), transcription levels are high and remain high. What function do IPTG and lactose share? How are they differently affected by the operon product? (need help with this question)

Lactose and IPTG affected by the operon are both inducers of the Lac-Operon. (is this correct)

3) What is “epigenetics”? What forms of gene regulation are usually involved in epigenetic control of a trait? Why do we have such a limited understanding of epigenetic processes? (need help with this question)

Epigenetics is the study of phenotype changes that do not change the DNA sequence. Genes can be turned on and off based on environment situations of past generations, (parents or even grandparents) were exposed. Examples of some environmental factors could be diet, stress, smoking, drinking alcohol, and diseases. Histone modification and methylation are usually involved in epigenetic control of a trait. (is this correct)

1.)A.)The lac operon is inducible by the presence of lactose. Loss-of-function mutations in the lacI gene, which encodes the lac repressor (pick all that apply):


A.)slow down the isomerization of lactose into allolactose
B.)decrease the amount of permease activity in the cell in the presence of lactose.
C.)prevent loss-of-function lacZ mutations from making the lac operon uninducible
D.)are recessive to wild type

B.)Mutations that eliminate the lacO operator site (pick all that apply):

A.)slow down the isomerization of lactose into allolactose
B.)decrease the amount of beta-galactosidase in the cell in the presence of lactose
C.)prevent lacS superrepressor mutations from making the lac operon uninducible
D.)are recessive to wild type

C.)Loss-of-function mutations in the lacZ gene, which encodes beta-galactosidase (pick all that apply):

A.)slow down the isomerization of lactose into allolactose
B.)decrease the amount of permease activity in the cell in the presence of lactose
C.)prevent lac repressor from binding the lacO operator site
D.)prevent IPTG from inducing the lac operon

D.)You are studying the Tory operon, which encodes the TorA and TorB genes, and is normally inducible by Torose. You find a mutation, m1, that causes the Tory operon to be uninducible. You examine the merodiploid (m1 TorA+ TorB-)/(+ ToryA- TorB+) and find that Tor A is uninducible and TorB is inducible. You conclude that:

A.)m1 acts in cis
B.)m1 acts in trans

In E.coli the lac operon is controlled by the presence or absence of both lactose and glucose. The lac repressor only allows expression in the presence of lactose, and it is also only activated when glucose levels are low, such that the lac operon is on when lactose is present but glucose is not.

You have cells that are mutant in the gene coding for the Lac repressor (I-). These cells lack the Lac repressor under all conditions. For these mutant cells, state whether the Lac operon will be switched on or off in the following situations, whether the lac repressor (I) is bound to the operator, and whether CAP-cAMP is bound upstream of the promoter.

a. in the presence of glucose and lactose

b. in the presence of glucose and the absence of lactose

c. in the absence of glucose and the absence of lactose

d. in the absence of glucose and the presence of lactose

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