Question: Explain why the events shown in part (
Explain why the events shown in part (a) inhibit transcription.
From Figure 15.15a:
Transcribed Image Text:
Enhancer CpG island Core promoter Coding sequence Activator - protein Methylation CH, CH, CH, CH, CH, CH, Methyl groups block the binding of an activator protein to an enhancer element
> Draw the structural feature of a dideoxyribonucleotide that causes chain termination. Explain how it does this.
> What is cDNA? In eukaryotes, how does cDNA differ from genomic DNA?
> Write a double-stranded DNA sequence that is 20 base pairs in length and is palindromic.
> What is a restriction enzyme? What structure does it recognize? What type of chemical bond does it cleave? Be as specific as possible.
> During which step of the reproductive cycle can a virus remain latent?
> According to the double-strand break model, does gene conversion necessarily involve DNA mismatch repair? Explain.
> What events does the RecA protein facilitate?
> In recombinant chromosomes, where is gene conversion likely to take place: near the breakpoint or far away from the breakpoint? Explain.
> Discuss three important advances that have resulted from gene cloning
> Is homologous recombination an example of mutation? Explain.
> What two molecular mechanisms can result in gene conversion? Do both occur in the double-strand break model?
> Which steps in the double-strand break model for recombination would be inhibited if the following proteins were missing? Explain the function of each protein required for the step that is inhibited. A. RecBCD B. RecA C. RecG D. RuvABC
> The molecular mechanism of SCE is similar to homologous recombination between homologs except that the two segments of DNA are sister chromatids instead of homologous chromatids. If branch migration occurs during SCE, will a heteroduplex be formed? Expla
> Describe the similarities and differences between homologous recombination involving sister chromatid exchange (SCE) and that involving homologs. Would you expect the same types of proteins to be involved in both processes? Explain.
> In Chapters 12 through 16, we discussed many sequences that are outside a coding sequence but are important for gene expression. Look up two of these sequences and write them out. Explain how a mutation could change these sequences, thereby altering gene
> If a mutation prevented IRP from binding to the IRE in the ferritin mRNA, how would the mutation affect the regulation of ferritin synthesis? Do you think there would be too much or too little ferritin?
> A point mutation occurs in the middle of the coding sequence for a gene. Which types of mutations—silent, missense, nonsense, and frameshift—would be most likely to disrupt protein function and which would be least likely?
> Is each of the following mutations a silent, missense, nonsense, or frameshift mutation? The original DNA strand is 5′–ATGGGACTAGATACC–3′. (Note: Only the coding strand is shown; the first codon is methionine.) A. 5′–ATGGGTCTAGATACC–3′ B. 5′–ATGCGACTAG
> Lactose permease is encoded by the lacY gene of the lac operon. Suppose a mutation occurred at codon 64 that changed the normal glycine codon into a valine codon. The mutant lactose permease is unable to function. However, a second mutation, which change
> X-rays strike a chromosome in a living cell and ultimately cause the cell to die. Did the X-rays produce a mutation? Explain why or why not.
> How would each of the following types of mutations affect protein function or the amount of functional protein that is expressed from a gene? A. Nonsense mutation B. Missense mutation C. Up promoter mutation D. Mutation that affects splicing
> What does a suppressor mutation suppress? What is the difference between an intragenic and an intergenic suppressor?
> Achondroplasia is a rare form of dwarfism. It is caused by an autosomal dominant mutation within a single gene. Among 1,422,000 live births, the number of babies born with achondroplasia was 31. Among those 31 babies, 18 of them had one parent with achon
> What is the difference between the mutation rate and the mutation frequency?
> With regard to TNRE, what is meant by the term anticipation?
> Trinucleotide repeat expansions (TNREs) are associated with several different human inherited diseases. Certain types of TNREs produce a long stretch of the amino acid glutamine within the encoded protein. When a TNRE exerts its detrimental effect by pro
> Why are insulators important for gene regulation in eukaryotes?
> What is the difference between an ancestral character and a shared derived character?
> If a mutagen causes bases to be removed from nucleotides within DNA, what repair system would fix this damage?
> Give an example of a mutagen that can change cytosine to uracil. Which DNA repair system(s) would be able to repair this defect?
> Are mutations random events? Explain your answer.
> A gene mutation changes an AT base pair to GC. This change causes a gene to encode a truncated protein that is nonfunctional. An organism that carries this mutation cannot survive at high temperatures. Make a list of all the genetic terms that could be u
> Distinguish between spontaneous and induced mutations. Which are more harmful? Which are avoidable?
> Explain what happens to the sequence of DNA during trinucleotide repeat expansion (TNRE). If someone was mildly affected with a TNRE disorder, what issues would be important when considering possible effects in future offspring?
> What type of mutation (transition, transversion, or frameshift) would you expect each of the following mutagens to cause? A. Nitrous acid B. 5-Bromouracil C. Proflavin
> Explain how a mutagen can interfere with DNA replication to cause a mutation. Give two examples.
> Make a drawing that shows how alkylating agents alter the structure of DNA, and explain the process.
> Discuss the consequences of a germ-line versus a somatic mutation.
> What is the difference between de novo methylation and maintenance methylation?
> As discussed in Chapter 25, most forms of cancer are caused by environmental agents that produce mutations in somatic cells. Is an individual with cancer considered a genetic mosaic? Explain why or why not.
> Which of the following mutations could be appropriately described as a position effect? A. A point mutation at the –10 position in the promoter region prevents transcription. B. A translocation places the coding sequence for a muscle-specific gene next
> Is a random mutation more likely to be beneficial or harmful? Explain your answer.
> Explain two ways that a chromosomal rearrangement can cause a position effect.
> Is each of the following mutations a transition, transversion, addition, or deletion? The original DNA strand is 5′–GGACTAGATAC–3′ (Note: Only the coding DNA strand is shown.) A. 5′–GAACTAGATAC–3′ B. 5′–GGACTAGAGAC–3′ C. 5′–GGACTAGTAC–3′ D. 5′–GGAG
> Describe how lytic bacteriophages are released from their host cells.
> What is the role of reverse transcriptase in the reproductive cycle of HIV and other retroviruses?
> Compare and contrast the entry step of the viral reproductive cycle of phage λ and HIV.
> Describe why the attachment step in a viral reproductive cycle is usually specific for one or just a few cell types.
> What do the terms host cell and host range mean?
> What is a viral envelope? Describe how it is made.
> In general, why is it important to regulate genes? Discuss examples of situations in which it would be advantageous for a bacterial cell to regulate genes.
> What is antisense RNA? How does it affect the translation of a complementary mRNA?
> Translational control is usually aimed at preventing the initiation of translation. With regard to cellular efficiency, why do you think this is the case?
> Mutations in tRNA genes can create tRNAs that recognize stop codons. Because stop codons are sometimes called nonsense codons, these types of mutations that affect tRNAs are called nonsense suppressors. For example, a normal tRNAGly has an anticodon sequ
> The combination of a 3–4 stem-loop and a U-rich attenuator in the trp operon (see Figure 14.12) is an example of a ρ-independent terminator. The function of ρ-independent terminators is described in Cha
> As described in Chapter 13, enzymes known as aminoacyl-tRNA synthetases are responsible for attaching amino acids to tRNAs. Let’s suppose that in a mutant bacterium tryptophanyl-tRNA synthetase has a reduced ability to attach tryptophan to tRNA: its acti
> As shown in Figure 14.12, four regions within the trpL mRNA can form stem-loops. Let’s suppose that mutations have been previously identified that prevent the ability of a particular region to form a stem-loop with a complementary regio
> What is meant by the term attenuation? Is it an example of gene regulation at the level of transcription or translation? Explain your answer.
> Would a mutation that inactivated lac repressor and prevented it from binding to the lac operator site result in the constitutive expression of the lac operon under all conditions? Explain. What is the disadvantage to the bacterium of having a constituti
> What features vary among different types of viruses?
> Mutations may have an effect on the expression of the lac operon and the trp operon. Would the following mutations have a cis- or transeffect on the expression of the protein-encoding genes in the operon? A. A mutation in the operator site that prevents
> What are the similarities and differences among viral genomes?
> What is diauxic growth? Explain the roles of cAMP and CAP in this process.
> What is the difference between a constitutive gene and a regulated gene?
> Explain the role of HIV protease during the process of HIV maturation.
> How does an HIV particle acquire its envelope?
> Describe the role of the Gag polyprotein during the assembly of HIV components at the host-cell plasma membrane.
> Compare and contrast the roles of fully spliced, incompletely spliced, and unspliced HIV RNA. Which type is needed in the early stages of HIV proliferation, and which is needed in later stages?
> Why is gap repair synthesis needed during HIV DNA integration?
> What is the role of the Vpr protein during the process of HIV DNA integration?
> Explain why histone eviction is needed for the elongation phase of transcription.
> Describe how HIV DNA is integrated into a chromosome of the host cell.
> Explain the role of RNase H (a component of reverse transcriptase) during the synthesis of HIV DNA.
> What structural features are common to all viruses? Which features are found only in certain types of viruses?
> Why is a host-cell tRNA needed for reverse transcription?
> Describe the process of reverse transcription of HIV RNA.
> Figure 18.11 shows a genetic switch that controls the choice between the lytic and lysogenic cycles of phage λ. What is a genetic switch? Compare the roles of a genetic switch and a simple operator site (like the one found in the
> In your own words, explain why it is necessary for the cI gene to have two promoters. What would happen if it had only PRE?
> How do the λ repressor and the cro protein affect the transcription from PR and PRM? Explain where these proteins are binding to cause their effects.
> With regard to promoting the lytic or lysogenic cycle, what would happen if the following genes were missing from the λ genome? A. cro B. cI C. cII D. int E. cII and cro
> Describe the role that integrase plays during the insertion of λ DNA into the host chromosome.
> Why is an NFR needed at the core promoter for transcription to occur?
> What key features distinguish the lytic from the lysogenic cycle?
> What is a prophage, a provirus, and an episome? What is their common role in a viral reproductive cycle?
> What is the difference between a temperate phage versus a virulent phage?
> Discuss why viruses are considered nonliving.
> Describe the structure of SRP in eukaryotes, and outline its role in targeting proteins to the ER membrane.
> Together with a specific set of proteins, snoRNAs direct the methylation or pseudouridylation of rRNAs. Does the snoRNA function as a scaffold, guide, ribozyme, blocker, decoy, and/or alterer of protein function or stability?
> What is the difference between an miRNA and an siRNA. How do these ncRNAs affect mRNAs?
> With regard to RNAi, what are three possible sources for doublestranded RNA?
> What is the phenomenon of RNA interference (RNAi)? During RNAi, explain how the double-stranded RNA is processed and how it leads to the silencing of a complementary mRNA.
> Explain how HOTAIR plays a role in the transcriptional regulation of particular genes.
> Describe two different ways that histone modifications may alter chromatin structure.
> What is meant by the term RNA world? Describe observations and evidence that support this hypothesized period of life on Earth. From the perspective of living cells, what are the advantages of having had the RNA world be superseded by a DNA/RNA/ protein
> Describe how the binding of iron regulatory protein to an IRE affects the mRNAs for ferritin and the transferrin receptor. How does iron (Fe3+) influence this process?
> What is a CpG island? Where would you expect one to be located? How does the methylation of CpG islands affect gene expression?
> Let’s suppose that a vertebrate organism carries a mutation that causes some cells that normally differentiate into nerve cells to differentiate into muscle cells. A molecular analysis reveals that this mutation is in a gene that encodes a DNA methyltran
> What is DNA methylation? When we say that DNA methylation is heritable, what do we mean? How is it passed from a mother to a daughter cell?
> What is an insulator? Describe two different ways that insulators may exert their effects.
> Histones are thought to be displaced as RNA polymerase is transcribing a gene. What would be the potentially harmful consequences if histones were not put back onto a gene after RNA polymerase had passed?
