Chapter 16: Problem 4
Describe the organization of the interphase nucleus. Include in your presentation a description of chromosome territories and interchromatin compartments.
Chapter 16: Problem 4
Describe the organization of the interphase nucleus. Include in your presentation a description of chromosome territories and interchromatin compartments.
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Get started for freeIn this chapter, we focused on the regulation of gene expression in eukaryotes. At the same time, we found many opportunities to consider the methods and reasoning by which much of this information was acquired. From the explanations given in the chapter: (a) How do we know that transcription and translation are spatially and temporally separated in eukaryotic cells? (b) How do we know that DNA methylation is associated with transcriptionally silent genes? (c) How do we know that core-promoter elements are important for transcription? (d) How do we know that the orientation of promoters relative to the transcription start site is important while enhancers are orientation independent? (e) How do we know that alternative splicing enables one gene to encode different isoforms with different functions? (f) How do we know that small noncoding RNA molecules can regulate gene expression?
Research indicates that promoters may fall into one of two classes: focused or dispersed. How do these classes differ, and which genes tend to be associated with each?
The regulation of mRNA decay relies heavily upon deadenylases and decapping enzymes. Explain how these classes of enzymes are critical to initiating mRNA decay.
Many viruses that infect eukaryotic cells express genes that alter the regulation of host gene expression to promote viral replication. For example, herpes simplex virus- 1 (HSV-1) expresses a protein called ICP0, which is necessary for successful viral infection and replication within the host. Lutz et al. (2017. Viruses 9: 210 ) showed that ICP0 can act as a ubiquitin ligase and target the redundant transcriptional repressors ZEB1 and ZEB2, which leads to upregulation of the miR-183 cluster (a set of three miRNAs transcribed from the same locus). (a) What likely happens to ZEB1 and ZEB2 upon HSV-1 infection? (b) How may ICP0 expression in a host cell lead to upregulation of the miR-183 cluster? (c) Speculate on how miR-183 cluster upregulation may benefit the virus.
Nonsense-mediated decay is an mRNA surveillance pathway that eliminates mRNAs with premature stop codons. How does the cell distinguish between normal mRNAs and those with a premature stop?
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