21. What are the similarities and differences between the lactase persistence mutations found in African populations and the one found in European populations? (Consider, for example, type of mutation, location, function.)
Q: Robert Bost and Richard Cribbs studied a strain of E. coli (araB14) that possessed a nonsense…
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Q: 20. Explain the effect of the mutation that occurs among northern European people on LCT gene…
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A: The correct answer is (d)single substitution.
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Q: 1. What are the main elements of the lac operon and their functions?
A: NOTE- Since you have posted multiple questions So we will be solving the first question for you. As…
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- 6. How do you know if the halibut you purchased at thesupermarket is really halibut? To identify the sourceof a biological sample, scientists PCR amplify andthen sequence a region of DNA known to vary between species. For animals, this DNA region is a648–base pair portion of the mitochondrial cytochrome oxidase I gene. The sequence of this mtDNAregion acts as a so-called DNA barcode because adatabase exists that contains the sequences of thismtDNA region that are unique for hundreds ofthousands of animal species.a. Why do you think that a region of mitochondrialDNA is used for barcoding animals, as opposed toa region of nuclear genomic DNA?b. A single pair of PCR primers can be used tobarcode any species of fish. Explain how this ispossible.c. List criteria that scientists would have consideredwhen determining which mitochondrial DNAsequence to use for barcoding animals.4. A recent estimate of the rate of base substitutions atSNP loci is about 1 × 10−8 per nucleotide pair pergamete.a. Based on this estimate, about how many de novomutations (that is, mutations not found in the genomes of your parents) are present in your own genome?b. Where and when did these de novo mutations inyour genome most likely occur?1. How would you determine experimentally mutagenesis caused by stress? 2. What are the evolutionary advantages associated with stress-induced mutagenesis? 3. How do bacteria cope with mutagenesis? List and explain at least three way
- 2. Null mutations are valuable genetic resources becausethey allow a researcher to determine what happens to anorganism in the complete absence of a particular protein. However, it is often not a trivial matter to determinewhether a mutation represents the null state of the gene.a. Geneticists sometimes use the following test forthe nullness of an allele in a diploid organism: If theabnormal phenotype seen in a homozygote for theallele is identical to that seen in a heterozygote(where one chromosome carries the allele in question and the homologous chromosome is known tobe completely deleted for the gene) then the alleleis null. What is the underlying rationale for thistest? What limitations might there be in interpreting such a result?1. What genetic changes can occur in bacteria to make them resistant to triclosan?2. How could the ability of bacteria to convert saturated fatty acids to unsaturated fatty acids be targeted by antibiotics?3. In a patient with tuberculosis carrying 1012 M. tuberculosis cells, (a) how many bacterial cells are expected to be resistant to isoniazid given a mutation rate of 1 in 108, and (b) how many bacterial cells are expected to be resistant to a combination of three antibiotics, assuming a similar mutation rate?4. Does the ability of cerulenin to stimulate fatty acid oxidation contribute to its antifungal effects?Robert Bost and Richard Cribbs studied a strain of E. coli (araB14)that possessed a nonsense mutation in the structural gene that encodes Lribulokinase,an enzyme that allows the bacteria to metabolize the sugararabinose (R. Bost and R. Cribbs. 1969. Genetics 62:1–8). From thearaB14 strain, they isolated some bacteria that possessed mutations thatcaused them to revert back to the wild type. Genetic analysis of theserevertants showed that they possessed two different suppressormutations. One suppressor mutation (R1) was linked to the originalmutation in L-ribulokinase and probably occurred at the same locus. Byitself, this mutation allowed the production of L-ribulokinase, but theenzyme produced was not as effective in metabolizing arabinose as theenzyme encoded by the wild-type allele. The second suppressormutation (SuB) was not linked to the original mutation. In conjunctionwith the R1 mutation, SuB allowed the production of L-ribulokinase, butSuB by itself was not able to suppress the…
- Robert Bost and Richard Cribbs studied a strain of E. coli (araB14) that possessed a nonsense mutation in the structural gene that encodes Lribulokinase, an enzyme that allows the bacteria to metabolize the sugar arabinose (R. Bost and R. Cribbs. 1969. Genetics 62:1–8). From the araB14 strain, they isolated some bacteria that possessed mutations that caused them to revert back to the wild type. Genetic analysis of these revertants showed that they possessed two different suppressor mutations. One suppressor mutation (R1) was linked to the original mutation in L-ribulokinase and probably occurred at the same locus. By itself, this mutation allowed the production of L-ribulokinase, but the enzyme produced was not as effective in metabolizing arabinose as the enzyme encoded by the wild-type allele. The second suppressor mutation (SuB) was not linked to the original mutation. In conjunction with the R1 mutation, SuB allowed the production of L-ribulokinase, but SuB by itself was not able…Robert Bost and Richard Cribbs studied a strain of E. coli (araB14) that possessed a nonsense mutation in the structural gene that encodes Lribulokinase, an enzyme that allows the bacteria to metabolize the sugar arabinose (R. Bost and R. Cribbs. 1969. Genetics 62:1–8). From the araB14 strain, they isolated some bacteria that possessed mutations that caused them to revert back to the wild type. Genetic analysis of these revertants showed that they possessed two different suppressor mutations. One suppressor mutation (R1) was linked to the original mutation in L-ribulokinase and probably occurred at the same locus. By itself, this mutation allowed the production of L-ribulokinase, but the enzyme produced was not as effective in metabolizing arabinose as the enzyme encoded by the wild-type allele. The second suppressor mutation (SuB) was not linked to the original mutation. In conjunction with the R1 mutation, SuB allowed the production of L-ribulokinase, but SuB by itself was not able…1. What are the genetic parameters in selecting a cattle bread for dairy production?
- 1. What can you conclude about the base composition and base distribution of G-C base pairs in the bandicootgenomic DNA from this result? Briefly explain how or why you would reach those conclusions.1. a)What would happen if the aminoacyl tRNA synthetase responsible for charging alanine tRNAs also charged methionine tRNAs with alanine? b)What would happen if an individual was homozygous for mutant alleles of the gene encoding the aminoacyl tRNA synthetase responsible for charging leucine tRNAs?2) How does the HAEIII enzyme discriminate between the C-G polymorphism in the TAS2R38 gene?
