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What is the major difference between qPCR and digital PCR?a. digital PCR is not quantitative b. digital PCR happens in silicoc. digital PCR separates the sample into thousands of subsamples for quantization making it more sensitive d. there is no difference

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*9.22 A central theme in genetics is that an organism's phenotype results from an interaction between its genotype and the environment. Because some diseases have strong environmental components, researchers have begun to assess how disease phenotypes arise from the interactions of genes with their environments, including the genetic background in which the genes are expressed. (See http://pga.tigr.org/desc.shtml for additional discussion.) How might DNA microarrays be useful in a functional genomic approach to understanding human diseases that have environmental components, such as somecancers?
9.26 Mycobacterium leprae is an intracellular bacterium that is the causative agent of leprosy, a chronic disease that infects the skin, nerves, and mucous membranes. It has not been possible to grow the bacterium in a culture medium, unlike its relative Mycobacterium tuberculosis, the causativeagent of tuberculosis (TB). M. tuberculosis can also grow intracellularly, as in the lungs it is taken up by alveolar macrophages and can multiply unchecked. The following table compares the genomes of these two organisms. M. leprae-M. tuberculosis:*Genome size (Mb): 3.27 -4.41*Percent of genome encodingproteins: 49.5 -90.8*Protein-coding genes (ORFs): - - 1,604- 3,959*Pseudogenes: 1,116- 6*Gene density (bp per gene): - - 2,037- 1,114*Average gene length: - 1,011-1,012a. Pseudogenes are nucleotide sequences that no longer produce functional gene products because they have accumulated inactivating mutations. Why might M. leprae have many more pseudogenes than M. tuberculosis?b. What analyses would you perform to understand how these two bacteria differ in terms of the enzymatic functions they can carry out?c. How might your analyses help you understand how to culture M. leprae?
9.14 After the gene for an autosomal dominant humandisease was identified, sequence analysis of the mutant allele revealed it to be a missense mutation. Two alternate hypotheses are proposed for how the mutant allele could cause disease. In one hypothesis, the missense mutation alters a critical amino acid in the protein so that the protein is no longer able to function: heterozygotes with just one copy of the normal allele develop the disease because they have half of the normal dose of this protein's function. In the second hypothesis, the missense mutation alters the protein so that it interferes with a normal process: heterozygotes develop the disease because the mutant allele actively disrupts a required function. How could you gather evidence to support one of these alternate hypotheses using knockout mice?

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