Bio 309 Exam 3 Study Guide
Bio 309 Exam 3 Study Guide BIOL 309
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This 6 page Study Guide was uploaded by Amanda Tobias on Tuesday May 10, 2016. The Study Guide belongs to BIOL 309 at Towson University taught by Dr. Masters in Spring 2016. Since its upload, it has received 105 views. For similar materials see Genetics in Biology at Towson University.
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Date Created: 05/10/16
1. Explain how the different properties of DNA, RNA and proteins affect their function. Why is DNA best for information storage? Why are proteins best for structural uses and catalytic function? Why has it been proposed that life started with RNA? DNA is stable and therefore is good for stability and information storage. The bases are also on the inside of the two strands so the information is protected. RNA is single stranded and is able to replicate itself. It is good for both structure and function and replication. The single strand has bases just like DNA so it is able to make a copy of itself and then make a copy of the copy. It can also fold into complex shapes because it is single stranded and can fold on to itself. Because it can self replicate and form complex structures, it is suggested that life started with RNA Proteins are by far the best for structural used and catalytic functions. They are single stranded and can form complex structures. They also are made of 20 chemically diverse amino acids so they can form many more diverse structures. 2. In what direction does DNA synthesis occur? In what direction is the template strand read during DNA synthesis? In what direction does RNA synthesis occur? In which direction is the template strand read during transcription? In what direction does translation occur? DNA synthesis occurs 5’ to 3’ The template strand in DNA synthesis is read 5’ to 3’ RNA synthesis occurs in the 5’ to 3’ direction During translation the strand is read in the 5’ to 3’ direction Translation occurs in the amino to carboxy direction 3. What is the error rate during DNA synthesis? What is the proofreading function, and how does it affect error rates? What is the error rate during transcription? Is there proofreading during transcription? What is the error rate during translation? Is there proofreading during translation? 5 6 The error rate for DNA synthesis is 10 to 10 The proofreading function recognizes an incorrect base that has been added and chews back to replace the incorrect base with the correct base. It lowers the error rate. 4. What affect does methylation of DNA have on mutation rates? Why? What sorts of sequences get methylated in the genome? What affect would sitespecific methylation have on transcription? Explain why global methylation can completely shut down transcription in eukaryotes but not prokaryotes. What role do histone deacetylases play in controlling gene expression? How about histone acetyl transferases? How about DNA methyl transferases? How about histone methyl transferases? Would global methylation at the 3’ end of a gene be likely to completely shut down transcription in eukaryotes? Methylation of DNA increases mutation rates, because 5 methyl cytosine deaminates to thymine. When that happens, the mismatch repair system has to guess which base is correct because cytosine and thymine are naturally found in DNA. If it guesses wrong, it will create a mutation. CG sequences get methylated Site specific methylation would decrease transcription, but it wouldn’t completely shut it off Global methylation can completely shut down transcription in eukaryotes but not prokaryotes because eukaryotes have histones and methylation causes them to bind more tightly to the DNA Histone deacetylase pushes you towards decreasing transcription Histone acetyl transferase pushes you toward increasing transcription DNA methyl transferase increases transcription Histone methyl transferase can increase or decrease transcription Global methylation at the 3’ end of a gene would completely shut down transcription 5. What is DNA methylation used for in organisms? Explain how inhibition of DNA methyl transferases could increase mutation rates. If methylation of a gene increased risk of cancer, what sort of gene would you predict it to be? DNA methylation is used to control gene expression Inhibition of DNA methyl transferases could increase mutations rates because it would decrease transcription and therefore increase methylation. When methylation is increased, mutation rate increases because 5 methyl cytosine deaminates to thymine, which causes mismatch repair to guess 6. Which are more common, transitions or transversions? Transitions 7. What are promoters? What are transcription factors? What are sigma factors? How many sigma factors are found in bacteria? What role do they play in controlling transcription? How many transcription factors are found in humans? In which groove of the DNA molecule would you expect a transcription factor to bind? Promoters are regions of the DNA that initiate transcription Transcription factors are proteins that bind to the DNA and help theRNA polymerase bind to the promoter Sigma factors are what transcription factors are called in prokaryotes There are 67 sigma factors in bacteria. Each sigma factor turns on and off a different gene and controls the expression of that gene There are a lot of transcription factors (~3000?) found in humans You would expect transcription factors to bind to the major groove 8. How do siRNA and miRNA affect gene expression? Do they affect the amount of transcription that occurs? Do they affect the amount of translation that occurs? They are short pieces of RNA that are complementary to an mRNA miRNA and siRNA are types of single stranded RNA that are small and they match with all or some of an mRNA sequence miRNA causes translational silencing(it is not a perfect match) and siRNA causes cleavage of the mRNA(it is a perfect match) They block expression of mRNA, and therefore decrease translation 9. Could mutations 5’ to the start of transcription affect mRNA stability? Could they affect transcription levels? Could mutations in sequences 3’ to the end of transcription affect transcription levels? Cold they cause complete silencing of transcription? Mutations 5’ to the start of transcription can’t affect mRNA stability Mutations 5’ to the start of transcription can affect transcription levels Mutations 3’ to the end of transcription can affect transcription levels Mutations 3’ to the end of transcription can’t cause complete silencing of transcription 10. Could mutations in the 5’utr region affect mRNA stability? Could they affect transcription levels? Could they affect translational efficiency? Could they disrupt the reading frame during translation? Could they affect protein structure? What about mutations in the 3’utr? Mutations in the 5’ utr can affect mRNA stability Mutations in the 5’ utr can affect translational efficiency Mutations in the 5’ utr can’t disrupt the reading frame during translation Mutations in the 5’ utr and 3’utr can’t affect protein structure 11. How do genome sizes and exome sizes compare across complex organisms? There is a lot of variation in genome sizes across complex organisms Complex organisms all have about the same size exome 12. How does translation initiate, what role does the 5’ cap play, and what happens when cap dependent translation is no longer possible? What role do the 5’ and 3’ UTRs play in controlling gene expression? Can the polyA tail play a role in initiating translation? Must the small ribosome binding site be 5’ to the start codon? What causes termination of translation? Translation initiates when the small ribosomal subunit binds to an AUG codon and establishes the reading frame. Translation begins after the large subunit also binds. The 5’ cap can be a binding site for the small subunit and also plays a role in stability When cap dependent translation is no longer possible, it can bind to the tail or the IRES sequence if there is one The polyA tail can also be a binding site for the small subunit The small ribosomebinding site doesn’t have to be 5’ to the start codon. The mRNA can fold and loop so that the subunit lines up where it is supposed to in order to begin translation Termination of translation occurs when the stop codon is in the reading frame 13. What is the nearly neutral theory of molecular evolution, and why does it have important consequences for small, isolated populations? Why do genomes expand in species with small effective population sizes? The nearly neutral theory of molecular evolution predicts that mutations behave close to neutrally if s,1/(eN ) where s is the selective disadvantage and Ne is the effective population size. Species with higher effective population sizes will be under much greater constraint This has important consequences for small isolated populations because a change in phenotype doesn’t have a big impact on fitness because of the lack of competition. Because of that, genome sizes can increase much more than in large populations. There can also be phenotypic issues within the population because mutations don’t decrease fitness, and those mutations will continue in the population. 14. What is linkage disequilibrium? If a mutation is recent, will it be in linkage disequilibrium? If a mutation is in linkage disequilibrium, does that mean it is recent? Linkage disequilibrium is when there is a nonrandom association of alleles If mutation is recent it will be in linkage disequilibrium If a mutation is in linkage disequilibrium that does not necessarily mean it is recent. It could be a region of the genome with a very low recombination rate, or the linkage could be conserved 15. What are tumor suppressors? What are oncogenes? If a mutation activates a gene, and makes cancer more likely, what kind of gene is it? Tumor suppressors are genes that when mutated fail to repress cancer. When not mutated, their job is repress and kill cancer like cells. Typically oncogenic transformation of tumor suppressor genes results in their inactivation. P53 is the typical tumor suppressor. Oncogenes are genes that when mutated actively promote cancer. Ras is an example If a mutation activates a gene and makes cancer more likely, it is a protooncogene 16. What happens when proteins misfold and why is that dangerous for cells? What fraction of proteins misfold? Explain how chaperone proteins could mask the effect of mutations. When proteins misfold, the hydrophobic regions are on the outside and the hydrophilic regions are on the inside They are toxic to cells because they can become prions, which recruit other normally folded proteins to misfold Chaperone proteins assist with folding the proteins, and are therefore able to prevent misfolding They can mask the effect of nonconservative mutations by how they fold the protein. Mutations in the amino acid sequence could code for a different folding of the protein, but chaperone proteins are able to fold it correctly 17. Explain how the design of the genetic code limits the impact of mutations. The genetic code minimizes the impact of mutations because of the way it is organized. Codons that differ in the third base position, or the wobble position of the codon often times code for the same amino acid or one similar in structure. Therefore, if there is a mutation in this position it doesn’t change the amino acid that is charged Bases in the third position of the codon are more likely to be silent, and transitions are more likely to be silent Conservative changes are when a mutation changes the amino acid that is charged, but it is one similar in structure Amino acids that are less harmful if a mutation were to add them in to a protein have more codons than amino acids that are harmful if mutated 18. Why does inbreeding reduce fitness? What two mechanisms have been proposed? The small population size allows for increase in mildly deleterious and harmful alleles. It will also result in decreased heterozygosity. Inbreeding depression has two possible mechanisms o Increase in genetic load (the expression of recessive deleterious allelels) o Loss of over dominance (over dominance is also known as hybrid vigor – an increased fitness from heterozygosity as opposed to the absence of harmful homozygosity) 19. What types of RNA are necessary for translation? mRNA tRNA rRNa 20. How does the stability of DNA, RNA and proteins compare? Is it necessary that replication occur shortly before transcription? Is it necessary that transcription occur shortly before translation? How about translation before replication? DNA is the most stable, and proteins and RNA vary in stability, but both are less stable than DNA It is not necessary that transcription occur shortly before translation. It just has to have occurred at some point It is necessary that translation occur shortly before replication because the proteins needed for replication to occur are made during translation and they have a short halflife. 21. Are there genes with microsatellites in their cisregulatory regions? What types of genes would you expect to have microsatellites in their ciscontrolling regions? There are genes with microsatellites in their cisregulatory regions Genes involved in fast adaptation such as behavior would be expected to have microsatellites in their cis controlling regions 22. You should be familiar with the concepts of polygenic traits, epistasis and pleiotropy. Could pleiotropy explain how an allele that reduced fitness with regard to a particular trait could persist in the population? Epistasis is when the phenotypic effect of a gene can be affected by another gene or genes. Most traits have many epistatic interactions Pleiotropy is when a single gene or locus can affect many things Most traits are actually determined by multiple locis and such traits are referred to as polygenic Pleitotropy can explain how an allele that reduced fitness could persist in the population because if that gene is determined by multiple loci, one combination could have a positive impact while another could be harmful. Because that allele is involved in both, it wouldn’t be eliminated from the population 23. Could overdominance explain how alleles that are selected against as homozygotes persist in a population? What would be an example? Overdominance can explain how alleles that are selected against as homozygotes persist in a population. Overdominance is the selective advantage of heterozygotes maintains genetic variability within populations Traits can’t be fixed. When heterozygotes breed 50% of the offspring will be homozygous for either trait The concept of overdominance can be extended to traits that are determined by hundreds of thousands of loci Perhaps it is a number of different particular combinations of alleles at many different loci that are selected for An example is sexual selection 24. What is frequency dependent selection? The selective advantage of rare genotype maintains genetic variability The left angled vs. right angled fish are an example 25. Suppose you could selectively increase the mutation rate in cancer cells. Might that be an effective cancer treatment? Ye, in order to become a cancer cell, a cell must undergo a lot of mutations. However, if the mutation rate becomes too high, it doesn’t become a cancer cell. It just becomes a mutant blob and dies. However, you don’t want to increase the mutation rate in normal cells because they would be more likely to become cancer cells so you have to make sure that the mutation rate is only increased in cancer cells. 26. Consider a type of cancer that is virtually unknown before the age of 50, but is quite common in persons above the age of 85. Would you expect the number of mutations necessary for this type of cancer to be higher, or lower, than what is necessary for leukemia? How would risk be distributed for this type of cancer? Would risk be more evenly distributed than is seen in leukemia? The number of mutations necessary for that type of cancer would be higher than the number of mutations needed for leukemia The risk for this type of cancer would be distributed unequally. Those people who have risk alleles would be at a much greater risk than those who don’t. Risk would not be more evenly distributed than is seen in leukemia 27. What type of protein is p53? How does it prevent cancer? P53 is a tumor suppressor gene It activates transcription of p21, which blocks progression through the G1/S checkpoint and activates transcription of Gadd45, which blocks progression through It responds to damage ot DNA and causes the cell to undergo apoptosis
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