Essentials of Genetics
9th Edition
ISBN: 9781292108933
Author: KLUG
Publisher: PEARSON
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Chapter 19, Problem 21PDQ
Yeager, M., et al.(Nature Genetics 39: 645–649, 2007) and Sladek, R. et al(Nature 445: 881–885, 2007) have used single-
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Describe how HpaII and MspI can be used to determine if a given DNA sequence is methylated. Any limitations associated with these enzymes in Amyloid-β alters the DNA methylation status of cell-fate genes in an Alzheimer’s disease model paper.
Taher, N., McKenzie, C., Garrett, R., Baker, M., Fox, N., & Isaacs, G. D. (2014). Amyloid-β alters the DNA methylation status of cell-fate genes in an Alzheimer’s disease model. Journal of Alzheimer’s Disease: JAD, 38(4), 831–844. https://doi.org/10.3233/JAD-131061
How does bisulfite treatment coupled with PCR enable the identification of DNA methylation? And, How could a Southern blot be used to determine if a given DNA sequence contains methylated CpGs in paper "Amyloid-β Alters the DNA Methylation Status of Cell-fate Genes in an Alzheimer's Disease Model."
Taher, N., McKenzie, C., Garrett, R., Baker, M., Fox, N., & Isaacs, G. D. (2014). Amyloid-β alters the DNA methylation status of cell-fate genes in an Alzheimer’s disease model. Journal of Alzheimer’s Disease: JAD, 38(4), 831–844. https://doi.org/10.3233/JAD-131061
Researchers in search of loci in the human genome that arelikely to contribute to the constellation of factors leading tohypertension have compared candidate loci in humans and rats[Stoll, M., et al. (2000). New Target Regions for Human Hypertensionvia Comparative Genomics. Genome Res. 10:473–482].Through this research, they identified 26 chromosomal regionsthat they consider likely to contain hypertension genes. Howcan comparative genomics aid in the identification of genesresponsible for such a complex human disease? The researchersstate that comparisons of rat and human candidate loci tothose in the mouse may help validate their studies. Why mightthis be so?
Chapter 19 Solutions
Essentials of Genetics
Ch. 19 - CASE STUDY| Cancer-killing bacteria Ralph, a...Ch. 19 - CASE STUDY| Cancer-killing bacteria Ralph, a...Ch. 19 - CASE STUDY |Cancer-killing bacteria Ralph, a...Ch. 19 - HOW DO WE KNOW? In this chapter, we focused on a...Ch. 19 - Prob. 2PDQCh. 19 - Why are most recombinant human proteins produced...Ch. 19 - Prob. 4PDQCh. 19 - One of the major causes of sickness, death, and...Ch. 19 - Prob. 6PDQCh. 19 - Sequencing the human genome and the development of...
Ch. 19 - Prob. 8PDQCh. 19 - As genetic testing becomes widespread, medical...Ch. 19 - What limits the use of differences in restriction...Ch. 19 - Might it make sense someday to sequence every...Ch. 19 - What is the main purpose of genome-wide...Ch. 19 - Prob. 13PDQCh. 19 - Prob. 14PDQCh. 19 -
15. In 2013 the actress Angelina Jolie elected to...Ch. 19 - Prob. 16PDQCh. 19 - Should the FDA regulate direct-to-consumer genetic...Ch. 19 - Prob. 18PDQCh. 19 - Prob. 19PDQCh. 19 - Private companies are now offering personal DNA...Ch. 19 - Yeager, M., et al.(Nature Genetics 39: 645–649,...Ch. 19 - In March 2010 Judge R. Sweet ruled to invalidate...
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- Comparisons between human and chimpanzee genomes indicate that a gene that may function as a wild-type or normal gene in one primate may function as a disease-causing gene in another [The Chimpanzee Sequencing and Analysis Consortium (2005). Nature 437:69–87]. For instance, the PPARG locus (regulator of adipocyte differentiation) is a wild-type allele in chimps but is clearly associated with Type 2 diabetes in humans. What factors might cause this apparent contradiction? Would you consider such apparent contradictions to be rare or common? What impact might such findings have on the use of comparative genomics to identify and design therapies for disease-causing genes in humans?arrow_forwardMutational signatures of p53 are shown in this image (G.P. Pfeifer et al., Nature, 21(48), 2002) for the three types of cancer with the highest death rates in the United States: lung (~225,000 deaths in 2016), breast (246,000), and colorectal (381,000). These data can be obtained by sequencing the gene that encodes p53. Approximately 85 percent of lung cancers occur in smokers. Based on these data, calculate how many deaths due to lung cancer among nonsmokers were reported in 2016. How much does smoking increase the likelihood of death due to lung cancer?arrow_forwardThe accompanying photo shows a sequencing gel from the original study that first sequenced the cystic fibrosis gene (J. R. Riordan et al. 1989. Science 245:1066–1073). From the photo, determine the sequence of the normal copy of the gene and the sequence of the mutated copy of the gene. Identify the location of the mutation that causes cystic fibrosis. (Hint: The CF mutation is a 3-bp deletion.)arrow_forward
- What is the first step in quantifying the relative amounts of mRNA in different tissues? Would this method be useful in determining which immune system genes might be over-expressed in severe Covid cases? Why or why not? Could quantitative PCR, which uses a DNA-binding dye, to show how many copies of the target DNA sequence could be used to quantify the amount of mRNA in a cell? Would you expect that a metabolically active tissue such as the liver would show more cDNA copies in such a method, compared to less metabolically active tissues such as skin cells? One reason that the types and amounts of mRNAs are quantified in different tissue types is to compare which genes are activated and which are inactive. It used to be thought that any gene that was transcribed was automatically translated. The discovery of RNA-degrading systems shows that the real situation in cells is more complemented. Do you believe that a larger amount of mRNA of a given type, say for alpha hemoglobin in…arrow_forwardBelow is a figure (here called Figure 1) from “Prognostic Significance of CpG Island Methylator Phenotype and Microsatellite Instability in Gastric Carcinoma,” by An et al., published in Clinical Cancer Research in 2005. The authors look at five microsatellite loci (BAT 25, BAT 26, D2S123, D5S346, and D17S250) in normal (N) and tumor (T) tissue from patients with Gastric Carcinoma. They amplify the loci by PCR and then instead of using standard agarose gel electrophoresis, they run the PCR products through capillary gel electrophoresis and detect bands as they pass a laser near the positive charge terminal. The x-axis in these plots is the time at which the band passed the laser (aka size of the PCR product) and the intensity of the peaks represents the amount of DNA in that band A. Which patient- 18, 30, or 1- shows the most microsatellite instability? Which patient shows the least? How do you know? B. In which repair pathway is it most likely that you will find the driver mutations…arrow_forwardwhich of the following statements about genome-wide association studies (GWAS) is correct? A) involves scanning the genomes of thousands of unrelated individuals with a particular mutation and comparing them with the genomes of individuals who do not have the mutation. B) involves scanning the genomes of thousands of unrelated individuals with a particular disease and comparing them with the genomes of individuals who do not have the disease C) attempt to identify genes that influence mutation risk D) attempt to identify genes that influence disease risk E) involves scanning the genomes of thousands of unrelated individuals with a particular disease and comparing them with the genomes of individuals who do not have the disease and GWAS attempt to identify genes that influence disease riskarrow_forward
- Why is QTL mapping in human genetic diseases important?arrow_forwardThe phenotype of a heterozygous mouse (Aa) is agouti. The agouti banding pattern is due to altered expression of the agouti gene. Which of the following statement is false? a) Expression of the agouti gene inhibits the production of eumelanin. b) Evidence suggests that the agouti gene is only expressed in tissues associated with fur production. c) Epigenetic markers silence the agouti gene resulting in dark pigmentation at the tip and root of the hair. d) All of the abovearrow_forward(6) Which of the following descriptions regarding human genetic variations is correct? A) Unlike rare variants, common variants have a frequency >5% and usually indicate low penetrance risk loci. B) Copy number variations frequently lead to decrease in gene expression. C) Both linkage analysis and association studies identify causal risk genetic variants. D) SNP is a common form of structural variation.arrow_forward
- A recent study examining the mutation rates of 5669 mammalian genes (17,208 sequences) indicates that, contrary to popular belief, mutation rates among lineages with vastly different generation lengths and physiological attributes are remarkably constant [Kumar, S., and Subramanian, S. (2002). Proc. Natl. Acad. Sci. USA 99:803–808]. The average rate is estimated at 12.2 * 10-9 per bp per year. What is the significance of this finding in terms of mammalian evolution?arrow_forwardWilliam Jeffrey and his colleagues crossed surface-dwelling Mexican tetras that had fully developed eyes with cave-dwelling blind Mexican tetras. The progeny from this cross had uniformly small eyes compared with those of surface fish (Y. Yamamoto, D. W. Stock, and W. R. Jeffrey. 2004. Nature 431:844–847). What prediction can you make about the expression of shh in these progeny at the embryonic stage relative to its expression in embryonic surface fish?arrow_forwardWhen the S.cerevisiae genome was sequenced and surveyed for possible genes, only about 40% of those genes had been previously identified in forward genetic screens. This left about 60% of predcited genes with no known function, leading some to dub the genes fun (function unknown) genes. a)As an approach to understanding the function of a certain fun gene, you wish to create a loss of function allele. How would you do this? b)You wish to know the physical location of the encoded protein product. How would you obtain such information?arrow_forward
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