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To analyze:
Plants of a particular species can either have the dominant wild-type
Using this information, answer the following:
Propose two mutational events that could cause the small DNA fragment that represents the mutant allele.
In northern blot analysis of mRNA, what mRNA differences would you anticipate for your two proposed mutational mechanisms?
Introduction:
The wild type dominant gene produces tall plants, and recessive genes are responsible for production of dwarf plants. The wild type gene gives a fragment of length around
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Chapter 10 Solutions
Genetic Analysis: An Integrated Approach (2nd Edition)
- A yeast geneticist irradiates haploid cells of a strain that is an adenine-requiring auxotrophic mutant, caused by mutation of the gene ade1. Millions of the irradiated cells are plated on minimal medium, and a small number of cells divide and produce prototrophic colonies. These colonies are crossed individually with a wildtype strain. Two types of results are obtained:(1) prototroph × wild type : progeny all prototrophic(2) prototroph × wild type : progeny 75% prototrophic, 25% adenine-requiring auxotrophsa. Explain the difference between these two types of results.b. Write the genotypes of the prototrophs in each case.c. What progeny phenotypes and ratios do you predict from crossing a prototroph of type 2 by the original ade1auxotroph?arrow_forwardThere are two genetic disorders that result from mutation in imprinted genes: Prader-Willi syndrome and Angelman syndrome. Prader-Willi syndrome results from deletion of region 15q11-q13, which in healthy individuals is a region imprinted such that only the paternal copy is expressed. In the pedigree above, individual I-1 is heterozygous for a deletion of region 15q11-q13 and does not have Prader-Willi syndrome. Individuals I-2 and II-1 are both homozygous wild type for the region. Which individuals in the pedigree might have Prader-Willi syndrome? (Who could potentially have the syndrome, based on what alleles it is possible for them to inherit and express?) Question 9 options: Only II-2 could have Prader-Willi syndrome III-1 could have Prader-Willi syndrome in the presented pedigree; II-2 could only have had it if she were male Both II-2 and III-1 could have Prader-Willi syndrome II-2 could have…arrow_forwardThe fruit fly Drosophila melanogaster has about 2 x 10^8 base pairs of DNA per haploid genome, of which about 75% in nonrepeated DNA. The DNA is distributed among four pairs of homologous chromosomes, which have a total of about 5,000 visible bands when in polytene forms in the salivary gland. The number of genes initially estimated from mutational studies was also about 5,000 but recent DNA sequencing studies suggest that the gene number may be somewhat higher. a. Why was it tempting to speculate that each band corresponds to a single gene? What does this suggest about the number of different proteins Drosophila can make? Does that seem like a reasonable number to you? b. Assuming all the nonrepeated DNA is uniformly distributed in the chromosomes, how much nonrepeated DNA (in base pairs) is there in average band?arrow_forward
- Consider two maize plants:a. Genotype C/cm ; Ac/Ac+, where cm is an unstableallele caused by a Ds insertionb. Genotype C/cm, where cm is an unstable allele causedby Ac insertionWhat phenotypes would be produced and in whatproportions when (1) each plant is crossed with a basepair-substitution mutant c/c and (2) the plant in part a iscrossed with the plant in part b? Assume that Ac and care unlinked, that the chromosome-breakage frequencyis negligible, and that mutant c /C is Ac+.arrow_forwardDuchenne Muscular Dystrophy (DMD) is a disorder that primarily affects the function of skeletal muscles used for movement and cardiac muscles used for heart beating. Dystrophin is a protein encoded by a single gene, DMD, that is expressed in skeletal and cardiac muscle. Some forms of muscular dystrophy may be caused by different mutations in the DNA sequence of the DMD gene. Because the DMD locus is on the X chromosome, males are affected at higher rates. Two brothers, one of whom has DMD and one of whom does not, worked with their genetic counselor (Links to an external site.) to have their DMD gene sequenced to identify genetic variation that may explain why one brother was affected and the other not. Because DMD is a very long gene, a fictionalized, simplified model of the results is presented here (Figure 1). The actual DMD mRNA is about 16,000 base-pairs!------Consider single nucleotide polymorphism (SNP) #1 (Figure 1). Is this mutation likely to cause Duchenne muscular…arrow_forwardTransgenic tobacco plants were obtained in which the vector Ti plasmid was designed to insert the gene of interest plus an adjacent kanamycin-resistance gene. The inheritance of chromosomal insertion was followed by testing progeny for kanamycin resistance. Two plants typified the results obtained generally. When plant 1 was backcrossed with wild-type tobacco, 50 percent of the progeny were kanamycin resistant and 50 percent were sensitive. When plant 2 was backcrossed with the wild type, 75 percent of the progeny were kanamycin resistant and 25 percent were sensitive. What must have been the difference between the two transgenic plants? What would you predict about the situation regarding the gene of interest?arrow_forward
- QUESTION 11 The location of five deletions have been mapped to a Drosophila chromosome, as shown in the following deletion map. Recessive mutations a, b, c, d and e are known to be located in the same region as the deletions but the order of the mutations on the chromosome is not known. Drosophila Chromosome Deletion 1 Deletion 2 Deletion 3 Deletion 4 Deletion 5 When flies homozygous for the recessive mutation are crossed with flies heterozygous for the deletions, the following results are obtained in which "m" represents recovery of flies with a mutant phenotype and "+" represents recovery of only flies with a wildtype phenotype. Use the data from the table below to determine the order of the genes (a-e) on the chromosome. Mutants Deletions a b C d e 1 + + + + m 2 + m + m 3 m m m m 4 + + m + + 5 m + m m + What is the gene order for these five genes? Please do not separate the letters representing the mutations with spaces or punctuation (e.g. LMNOP)arrow_forwardThe DNA of every individual in the pedigree shown in image B (below) has been sequenced at the causative locus, all the non- shaded individuals are wild type apart from III.1 and III.6. III.1 and III.6 have both been proven to have the causative allele for the condition but they do not exhibit any of the phenotypic signs or symptoms. Based on this pedigree, what is the level of penetrance for the condition? Please give your answer as a percentage to one decimal place, give the number only, no percentage symbol. ANSWER: Given the information above I calculate the level of penetrance seen in image B to be Blank 1 percent. A KEY Homozygous Homozygous Heterozygous Heterozygous Wild Type Male Female Male Female Male Note: Completely red symbol denotes an individual exhibiting the phenotype of interest CI || III IV V 1/4 1/2 1/2 1/2 1/2 Wild Type Female 1/4 1/2 Affected Known carrier Affected female Normal female Affected male Normal male D ●●●arrow_forwardThe wild-type (normal) fruit fly, Drosophila melanogaster, has straight wings and long bristles. Mutant strains have been isolated with either curled wings or short bristles. The genes representing these two mutant traits are located on separate chromosomes. Carefully examine the data from the five crosses below. (a) For each mutation, determine whether it is dominant or recessive. In each case, identify which crosses support your answer; and (b) define gene symbols and determine the genotypes of the parents for each cross. Cross 1. straight, short X straight, short 2. straight, long X straight, long 3. curled, long X straight, short 4. straight, short X straight, short 5. curled, short X straight, short straight wings, long bristles 30 120 40 40 20 Number of Progeny straight curled wings, wings, short long bristles bristles 90 10 0 40 120 60 40 40 0 20 curled wings, short bristles 30 0 40 0 60arrow_forward
- Friedreich ataxia (FRDA) is an autosomal recessive, neurodegenerative disease that causes a lack of voluntary coordination of muscle movements. Affected individuals are homozygous for an unusually large number (expansion) of repeats of a trinucleotide sequence (GAA) in the first intron of the X25 gene. Unaffected individuals typically have between 7 and 38 repeats of the trinucleotide (GAAGAAGAAGAA…). FRDA patients have anywhere from 66 to over 1,700 repeats. To understand how the GAA trinucleotide expansion leads to FRDA, researchers looked at X25 gene expression by extracting RNA from affected and unaffected patients and doing a northern blot analysis (see the figure below): In panel “a,” the researchers used a probe to detect X25 mRNA. In panel “b,” the researchers used a probe on a duplicate of the original blot to detect human GAPDH mRNA (GAPDH is an enzyme involved in glycolysis). The sample labeled “YR” is mRNA from yeast cells that was used as a control. Explain…arrow_forwardIn McCune-Albright syndrome, fibrous connective tissue replaces bone, tan patches (café-au-lait spots) dot the skin, and hormone abnormalities cause early puberty and malfunction of the thyroid, pituitary, and adrenal glands. The phenotype is highly variable, and all patients are somatic mosaics for the mutation, which is in the gene GNAS1. Why is the condition seen only in mosaics?arrow_forwardthis is what i have said about this image so far, what else can be said aswell including the raw count column. " Interpreting the results of an RNA-Seq analysis is pivotal in understanding the underlying genetic mechanisms of diseases such as breast cancer. In this analysis, Figure 1 provides comprehensive data on differentially expressed genes associated with breast cancer. By delving into the provided information, we can gain valuable insights into the molecular landscape of this disease. First focus is on the gene with the highest fold change, EYA4, situated on chromosome 6. With a staggering fold change of 3604.4176, EYA4 exhibits an unprecedented level of overexpression in cancerous cells compared to normal cells. This profound alteration suggests a pivotal role for EYA4 in breast cancer pathogenesis. The log2 fold change of 11.81555 further emphasizes the magnitude of this difference in gene expression. Statistical significance is evident, with an exceptionally low p-value of…arrow_forward
- Human Heredity: Principles and Issues (MindTap Co...BiologyISBN:9781305251052Author:Michael CummingsPublisher:Cengage Learning
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