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Seven deletion mutations are tested for their ability to form wild-type recombinants with five point mutations as shown in the table below:
Deletion mutation | |||||||
Point mutation | |||||||
a | - | + | - | - | + | + | - |
b | + | + | + | - | + | - | - |
c | + | + | + | + | - | - | - |
d | - | + | + | - | + | - | - |
e | + | - | - | - | + | + | - |
Using the data from the table, construct a genetic map of the order of point mutations and indicate the segment deleted by each deletion mutation.
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Chapter 6 Solutions
Genetic Analysis: An Integrated Approach (3rd Edition)
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- Compared to the normal A allele, the disease-causing allele in sickle cell anemia (S allele) is missing an MstII restriction site. On a Southern blot of genomic DNA cut with MstII and hybridized with the probe shown on the diagram below, a person with sickle anemia, carrying two S alleles, will show Choose an answer below: a single band at 1.1 kb. a single band at 1.3 kb. a single band at 0.2 kb. one band at 0.2 and one at 1.3 kb. one band at 1.1 and one at 1.3 kb.arrow_forwardA 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?arrow_forwardHydroxylamine (HA) causes only G • C → A • T transitions in DNA. Will HA produce nonsense mutations in wild-type strains?arrow_forward
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