You are studying celiacs disease and have identified a potential gene for the disease using linkage analysis. You decide to test your hypothesis by making transgenic mice that carry a nonsense mutation in the candidate gene you have identified to see if they develop a phenotype similar to that found in Celiacs disease What sort or experimental approach are you using when you test your gene in your mouse model? a. Reverse genetic b. Quantitative genetic C. Forward genetic D.Expression analysis E. None of the above

You are studying celiacs disease and have identified a potential gene for the disease using linkage analysis. You decide to test your hypothesis by making transgenic mice that carry a nonsense mutation in the candidate gene you have identified to see if they develop a phenotype similar to that found in Celiacs disease What sort or experimental approach are you using when you test your gene in your mouse model? a. Reverse genetic b. Quantitative genetic C. Forward genetic D.Expression analysis E. None of the above

Human Heredity: Principles and Issues (MindTap Course List)

11th Edition

ISBN:9781305251052

Author:Michael Cummings

Publisher:Michael Cummings

Chapter15: Genomes And Genomics

Section: Chapter Questions

Problem 14QP

See similar textbooks

Similar questions

Mouse models for human genetic diseases are potentially powerful tools to help geneticists understand thecause of the aberrant phenotypes and develop newtherapeutic measures. However, such mice are not always as useful to investigators as it might seem at firstglance. Suppose that you have a mouse knockoutmodel for a human disease caused by homozygosityfor a null allele of a gene. Discuss how the followingsituations might complicate investigations of the human disease based on this mouse model.a. Mice have a shorter life span than humans.b. Mice homozygous for certain knockout mutationsdie in utero.c. Mouse genomes may have additional copies of thegene whose mutation causes the disease in humans.
Mouse models for human genetic diseases are potentially powerful tools to help geneticists understand thecause of the aberrant phenotypes and develop newtherapeutic measures. However, such mice are not always as useful to investigators as it might seem at firstglance. Suppose that you have a mouse knockoutmodel for a human disease caused by homozygosityfor a null allele of a gene. Discuss how the followingsituations might complicate investigations of the human disease based on this mouse model.a. Mice have a shorter life span than humans.b. Mice homozygous for certain knockout mutationsdie in utero.c. Mouse genomes may have additional copies of thegene whose mutation causes the disease in humans.d. Mice from different inbred lines homozygous forthe same gene knockout vary in the penetrance andexpressivity of the phenotype.e. Manipulations to create the knockout mouse, suchas the presence of a drug resistance gene that allowsthe selection of cells containing the knockout (seeFig. 18.9),…
Suppose that you could undergo genetic testing at age 18 for susceptibility to a genetic disease that would not appear until middle age and has no available treatment. a. What would be some of the possible reasons for having such a genetic test and some of the possible reasons for not having the test? b. Would you personally want to be tested? Explain your reasoning.
Give a schematic diagram of how we can Treatment Down's syndrome by using gene therapy? Please answer at your own words,please..
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?
You are a developmental geneticist studying flowering time variation in Arabidopsis. You perform a mutagenesis screen to identify mutants in the photoperiod pathway. You conduct the screen and find two different plants that show the same mutant phenotype. You then use a complementation test. What is the predicted outcome of this test if both phenotypes are caused by mutations in separate genes? recover the wild type phenotype overexpress the gene O recover the mutant phenotype
Give a schematic diagram of how we can Treatment Down Syndrome by using gene therapy? Please answer at your own words,please..
As an alternative to random mutagenesis, scientistscan screen for mutant phenotypes by knocking downindividual gene functions systematically using RNAi.a. Suggest ways to construct transgenes that in flieswould express RNAi to knock down a gene.b. How could you perform a mutant screen for fly genesrequired for wing development using RNAi? Howcould this screen avoid the problem of pleiotropy?
A paper hypothesizes that white flowers are unable to produce anthocyanins (purple pigments) because they lack a functional “A” protein. However, it is also possible that an unknown gene is responsible for the lack of anthocyanins. Now that they have isolated DNA sequences of the “A” allele, design an experiment to use these DNA sequences to distinguish between these two hypotheses.
As a molecular biologist and horticulturist specializing in snapdragons, you have decided that you need tomake a genomic library to characterize the flowercolor genes of snapdragons.a. How many genomic equivalents would you like tohave represented in your library to be 95% confident of having a clone containing each gene inyour library?b. How do you determine the number of independentclones that should be screened to guarantee thisnumber of genomic equivalents?
describe two blotting methods (i.e., Northern blottingand Western blotting) used to detect gene products. Northern blotting detects RNA and Western blotting detects proteins. Supposethat a female fruit fly is heterozygous for a maternal effect gene,which we will call gene B. The female is Bb. The normal allele, B,encodes a functional mRNA that is 550 nucleotides long. A recessive allele, b, encodes a shorter mRNA that is 375 nucleotideslong. (Allele b is due to a deletion within this gene.) How couldyou use one or more of these techniques to show that nurse cellstransfer gene products from gene B to developing oocytes? Youmay assume that you can dissect the ovaries of fruit flies and isolate oocytes separately from nurse cells. In your answer, describeyour expected results.
a. Describe two ways you could potentially make atransgene that would inhibit the function of a specific gene in a transgenic organism. (Hint: For oneof these techniques, recall the discussion of RNAinterference in Chapter 17.)b. Discuss how you could use either of these methodsto construct a mouse model for a recessive humangenetic condition associated with a loss of function, such as cystic fibrosis.