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Transcript
Chapter 19: Control of Gene Expression in Eukaryotes Text Vocabulary: Differential Gene Expression Chromatin Chromatin Remodeling RNA Processing Histrones Nucleosomes DNA Methylation Histone Code Histone Acetyltransferases Histone Deacetyltransferases Acetylation Chromatin-remodeling Complexes Epigenetic Inheritance Promoter TATA Box TATA-binding Proteins Regulatory Sequences Promoter-proximal Elements Enhancers Transcriptional Activators Silencers Repressors Regulatory Transcription Factors Transcription Factor Basal Transcription Factor Spliceosomes Alternative Splicing RNA Interference microRNA (miRNA) Proteasome Tumor Suppressor Proto-oncogenes Oncogenes P53 Lecture 25 “Control of Gene Expression in Eukaryotes: Part 1” PPT Review 1.) What are the different levels at which control of eukaryotic genes can occur? a. Can occur at: 2.) What problem with the eukaryotic genome did the discovery of chromatin solve? 3.) What are histones? What are nucleosomes? 4.) What is the gene promoter? In order for RNA Polymerase to gain access to the promoter, what state must chromatin be in? 5.) What are the 3 ways (from lecture) that chromatin can be altered? 6.) What is acetylation? How can does acetylation of histones affect chromatin structure? What enzymes catalyze this? 7.) What is a promoter proximal element? How does it differ from the gene’s promoter? What is the benefit of the promoter proximal elements for gene expression? 8.) What are the steps for transcription initiation in eukaryotes? 9.) What is a transcriptional enhancer? How enhancers in the DNA work from such far distances? Lecture 26 “Control of Gene Expression in Eukaryotes: Part 2” PPT Review 1.) Is the final mature mRNA transcript composed of exons or introns? What occurs during splicing of primary mRNAs? 2.) What is alternative splicing? How is alternative splicing controlled? 3.) What are microRNAs (miRNAs)? What post-transcriptional process are they involved in? What protein complex do miRNAs interact with during this process? 4.) What are the steps in the post-transcriptional regulatory process that miRNAs are involved in? 5.) Why is RNAi also referred to as gene knockdown? 6.) What is a tumor suppressor gene? Why are they associated with cancer? What example of a tumor suppressor did we talk about in lecture? 7.) What effect might too much HDAC have on 1.) expression of p53 and 2.) the cell cycle? 8.) What is a proto-oncogene? How does it differ from an oncogene? 9.) What effect might too much HAT have on 1.) expression of a proto-oncogene and 2.) the cell cycle? 10.) How can translation be slowed or stopped (ex. From class)? What type of scenario could this occur in? Why might it be useful to the cell to stop most protein synthesis in these conditions?
