Question: Figure 18.11 shows a genetic switch
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 lac operon) in gene regulation. From Figure 18.11: 
Transcribed Image Text:
OR 5 3 3 ORs Oa Om Pum During the lysogenic cycle, the A repressor controls During the lytic cycle, the cro protein controls the switch. the switch. cro protein binds to Os The A repressor binds to O -A repressor cro protein Os Og2 O Ons Ora Oen PeM PR Pe ZOff On cro protein binds to Oga and Ogt The A repressor binds to Ona and then to Ors Ons Ora Oen Ops Og2 Pe The amount of the A repressor Pe falls, because cll is not o activating PRe- The i repressor is released from Ogs Off Lytic cycle occurs Ona Ona Om Lysogenic cycle occurs en in
> 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?
> Explain why the events shown in part (a) inhibit transcription. From Figure 15.15a: 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
> 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.
> 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?
> What is a nucleosome-free region? Where are such regions typically found in a genome? How are nucleosome-free regions thought to be functionally important?
> What is meant by the term histone code? With regard to gene regulation, what is the proposed role of the histone code?
> An ncRNA may have the following functions: scaffold, guide, alterer of protein function or stability, ribozyme, blocker, and/or decoy. Which of those functions is/are mediated by each of the ncRNAs listed next? (Note: A single ncRNA may have more than on
> What are the two ways in which piRNAs and PIWI proteins prevent the movement of transposable elements?
> Explain how the acetylation of core histones may loosen chromatin packing.
> What is a histone variant?
> Explain how the VIN3/PRC2 complex specifically binds to the FLC gene.
> Explain how the miR-200 family of miRNAs behave as tumorsuppressor genes. What happens when their expression is blocked or decreased?
> List five types of cancer in which ncRNAs can be involved.
> Outline the steps that occur when piRISCs silence transposable elements by repressing transcription and by directly inhibiting TE RNAs. What is the role of piRNAs in this process?
> What are the roles of Cas1, Cas2, and Cas9 proteins in bacterial genome defense?
> In the CRISPR-Cas system, does the tracrRNA act as a scaffold, guide, ribozyme, blocker, decoy, and/or alterer of protein function or stability?
> Compare and contrast the roles of crRNA and tracrRNA in the defense process against bacteriophages provided by the CRISPRCas system.
> Look at Figure 17.6 and predict what would happen if the SRP RNA was unable to stimulate the GTPase activities of the GTPbinding proteins within SRP and the SRP receptor. From Figure 17.6: Ribosome 5' 3' ER signal sequence NH, As a polypeptide is b
> Which component of the CRISPR-Cas system directly recognizes the bacteriophage DNA?
> List and briefly describe four types of molecules that can bind to an ncRNA.
> In general, explain how epigenetic modifications are an important mechanism for developmental changes that lead to specialized body parts and cell types. How do the trithorax and polycomb group complexes participate in this process?
> Following X-chromosome inactivation, most of the genes on the inactivated X chromosome are silenced. Explain how. Name one gene that is not silenced.
> Outline the molecular steps in the process of X-chromosome inactivation (XCI). Which step plays a key role in choosing which of the X chromosomes will remain active and which will be inactivated?
> Let’s suppose a mutation removes the ICR next to the Igf2 gene. If this mutation is inherited from the mother, will the Igf2 gene (from the mother) be silenced or expressed? Explain.
> Explain how DNA methylation and the formation of a DNA loop control the expression of the Igf2 gene in mammals. How is this gene imprinted so that only the paternal copy is expressed in offspring?
> What is the key difference between cis- and trans-epigenetic mechanisms for maintaining an epigenetic modification? In Chapter 5, we considered genomic imprinting of the Igf2 gene, in which offspring express the copy of the gene they inherit from their f
> Explain how epigenetic changes may be targeted to specific genes.
> List and briefly describe five types of molecular mechanisms that may underlie epigenetic gene regulation.
> If a winter-annual strain of Arabidopsis is grown in a greenhouse and not exposed to cold temperatures, its ability to flower is inhibited. Which gene is responsible for this inhibition?
> Why is GTP necessary for this process?
> Is paramutation a cis- or a trans-epigenetic mechanism?
> How can environmental agents that do not cause gene mutations contribute to cancer? Would these epigenetic changes be passed to offspring?
