Exam 18: Control of Gene Expression in Eukaryotes

The primary difference between an enhancer and a promoter-proximal element is that _____.

The normal function of a tumor suppressor gene is to _____.

Imagine you've isolated a yeast mutant that contains histones resistant to acetylation.What phenotype do you predict for this mutant?

Not long ago,it was believed that a count of the number of protein-coding genes would provide a count of the number of proteins produced in any given eukaryotic species.This is incorrect,largely due to the discovery of widespread _____.

Imagine that you are studying the control of β-globin gene expression in immature red blood cells (mature red blood cells contain β-globin protein but lack a nucleus and therefore the β-globin gene).If you deleted a sequence of DNA outside the protein-coding region of the β-globin gene and found that this increased the rate of transcription,the deleted sequence likely functions as a(n)_____.

Gene expression is often assayed by measuring the level of mRNA produced from a gene.If one is interested in knowing the amount of a final active gene product,a potential problem of this method is that it ignores the possibility of _____.

An example of a basal transcription factor is _____.

Which of the following allows more than one type of protein to be produced from one gene?

p53 activates genes that _____.

How do chromatin-remodeling complexes recognize the genes they should act on?

In the experiment shown in the figure above,Tonegawa and his colleagues were able to express β-globin in an antibody-producing cell that normally does not express β-globin.They achieved this result by splicing an enhancer from an antibody-producing gene into the protein-coding portion of the β-globin gene.They then introduced this recombinant gene into cultured antibody-producing cells.Why was the choice of antibody-producing cells rather than,say,muscle or skin cells critical for the success of this experiment?

Which of the following is false?

Which of the following types of mutation would convert a proto-oncogene into an oncogene?

The authors state: "In this study,we report that,in the absence of neuronal activity,MeCP2 binds specifically to BDNF promoter III and functions as a negative regulator of BDNF expression.In response to neuronal activity-dependent calcium influx into neurons,MeCP2 becomes phosphorylated and is released from the BDNF promoter,thereby permitting BDNF promoter III-dependent transcription." Reading this statement in isolation,it would be easy to have the impression that MeCP2 works as a negatively acting transcription factor.However,based on the summary of the paper provided above,MeCP2 acts as a _____.

Imagine you've isolated a yeast mutant that contains a constitutively (constantly)active histone deacetylase.What phenotype do you predict for this mutant?

If the DNA sequence was substantially altered from one of the following,which would prevent the binding of the TATA-binding protein (TBP)?

Ovalbumin,the major protein of egg white,is secreted by cells that line the oviduct as the bird egg moves down the oviduct.Imagine you're repeating the classic Weintraub-Groudine experiment,but with a twist: You're assaying the DNase sensitivity of the promoter regions of the β-globin and ovalbumin genes in oviduct cells of laying hens.In this case you expect to find that _____.

If a biologist wanted to analyze the evolutionary relationship in a gene type that is found in both eukaryotes and bacteria,which of the following would NOT be useful?

Predict what would occur in the experiment shown in Figure 18.1 if Tonegawa and colleagues had mistakenly inserted the antibody gene enhancer in reverse orientation (backward)into the β-globin gene.

The B-I mutation in anthocyanin (red pigments)produces pigmented corn plants,whereas the B′ mutation in the same gene produces nearly unpigmented corn plants.Normally,when B-I is crossed with recessive colorless alleles of the b gene,the resulting plants are pigmented.However,when B-I and B′ plants are intercrossed,the F₁ plants are essentially unpigmented,like the B′ homozygotes.Thus,B-I is altered by being in the same genome as B′.If this outcome were due simply to the dominance of B′ to B-I,then a self-cross of the F₁ plants should generate B-I-colored homozygotes as approximately 1/4 of the F₂ progeny.Instead,no F₂ are pigmented.Intercrosses of the F₂ and of further generations do not restore the pigmented phenotype.What is the term for this type of inheritance?