Correct answers already provided! Please don't just tell me the answers bc I know them already. Help me with my own question.I get everything else in this problem other than the third option: Introduce the mutant human HD allele as a transgene into the mouse genome with transgene integration anywhere in the mouse genome.Why is the first question (left) okay with introducing mutant human HD allele and the second question (right) is not? I heard that introducing allele without using CRISPR-Cas9 is very rare and difficult. If so, how does it work in the first problem (Hungtinton's chorea)? You would like to create a mouse model for spinal muscular atrophy, a recessive human disease caused by a loss of functionYou would like to create a mouse model of the human disease Huntington's chorea, a dominant disease caused by a gain of mutation in the SMN1 gene. Which of the following strategies would be suitable? Select all that applyfunction mutation in the human HD gene. Which of the following strategies would be suitable? Select all that applyUse CRISPR-Cas9 technology to cut the mouse HD gene; supply the mutant human HD allele as a repair templateand select for transgenics where the the mutant human HD replaced the mouse HD geneUse CRISPR-Cas9 to introduce frameshift mutations in the mouse HD gene; breed the resulting mutant mice togenerate homozygous mutantsIntroduce the mutant human HD allele as a transgene into the mouse genome with transgene integrationanywhere in the mouse genomeIntroduce the wild type human HD allele as a transgene into mouse genome; select transgenics where humanHD replaced the wild type mouse HD gene via homologous recombinationUse CRISPR-Cas9 to introduce frameshift mutations in the mouse SMN1 gene; breed the resulting mutant mice togenerate homozygous mutantsUse CRISPR-Cas9 technology to cut the mouse SMN1 gene; supply a mutant human SMN1 allele as a repairtemplate and select for transgenics where the the human allele replaced the mouse allele of SMN1; breed theresulting mutant mice to generate homozygous mutantsIntroduce a mutant human SMN1 allele as a transgene into mice, with transgene integration anywhere in themouse genome; breed the resulting transgenics to generate homozygotesIntroduce a wild type (functional) human SMN1 allele as a transgene into mice; select transgenics where thehuman gene replaced the wild type mouse SMN1 gene via homologous recombination

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Human Anatomy & Physiology (11th Edition)

11th Edition

ISBN:9780134580999

Author:Elaine N. Marieb, Katja N. Hoehn

Publisher:Elaine N. Marieb, Katja N. Hoehn

Chapter1: The Human Body: An Orientation

Section: Chapter Questions

Problem 1RQ: The correct sequence of levels forming the structural hierarchy is A. (a) organ, organ system,...

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Correct answers already provided! Please don't just tell me the answers bc I know them already. Help me with my own question.

I get everything else in this problem other than the third option: Introduce the mutant human HD allele as a transgene into the mouse genome with transgene integration anywhere in the mouse genome.

Why is the first question (left) okay with introducing mutant human HD allele and the second question (right) is not? I heard that introducing allele without using CRISPR-Cas9 is very rare and difficult. If so, how does it work in the first problem (Hungtinton's chorea)?

You would like to create a mouse model for spinal muscular atrophy, a recessive human disease caused by a loss of function
You would like to create a mouse model of the human disease Huntington's chorea, a dominant disease caused by a gain of mutation in the SMN1 gene. Which of the following strategies would be suitable? Select all that apply
function mutation in the human HD gene. Which of the following strategies would be suitable? Select all that apply
Use CRISPR-Cas9 technology to cut the mouse HD gene; supply the mutant human HD allele as a repair template
and select for transgenics where the the mutant human HD replaced the mouse HD gene
Use CRISPR-Cas9 to introduce frameshift mutations in the mouse HD gene; breed the resulting mutant mice to
generate homozygous mutants
Introduce the mutant human HD allele as a transgene into the mouse genome with transgene integration
anywhere in the mouse genome
Introduce the wild type human HD allele as a transgene into mouse genome; select transgenics where human
HD replaced the wild type mouse HD gene via homologous recombination
Use CRISPR-Cas9 to introduce frameshift mutations in the mouse SMN1 gene; breed the resulting mutant mice to
generate homozygous mutants
Use CRISPR-Cas9 technology to cut the mouse SMN1 gene; supply a mutant human SMN1 allele as a repair
template and select for transgenics where the the human allele replaced the mouse allele of SMN1; breed the
resulting mutant mice to generate homozygous mutants
Introduce a mutant human SMN1 allele as a transgene into mice, with transgene integration anywhere in the
mouse genome; breed the resulting transgenics to generate homozygotes
Introduce a wild type (functional) human SMN1 allele as a transgene into mice; select transgenics where the
human gene replaced the wild type mouse SMN1 gene via homologous recombination

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Step 1: Introduction

In the realm of genetic research, producing accurate animal models of human diseases is essential for understanding these conditions and coming up with new remedies. In order to recreate the genetic changes that cause human diseases, this frequently entails modifying the genes of animals, such as mice. However, depending on the nature of the disease itself, the methods employed to develop these models can differ greatly. In this context, we examine the differences between Huntington's chorea and spinal muscular atrophy (SMA), two hereditary disorders, and the precise genetic engineering techniques necessary to simulate them in mice. These variations underline how crucial it is to adapt genetic strategies to the particular traits of each disease.

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