ction mutation in the SMNT gene. which of the following strategies would be suitable? Select all that apply 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 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 O 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 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

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,...
icon
Related questions
Question

11,12

You would like to create a mouse model for spinal muscular atrophy, a recessive human disease caused by a loss of
function mutation in the SMN1 gene. Which of the following strategies would be suitable? Select all that apply
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
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 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
Transcribed Image Text:You would like to create a mouse model for spinal muscular atrophy, a recessive human disease caused by a loss of function mutation in the SMN1 gene. Which of the following strategies would be suitable? Select all that apply 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 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 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
You are interested in studying the FBN1 gene, a candidate identified via GWAS for a gene involved in heritable risk of heart
disease. You have a human cardiac myocyte cell line with wild type alleles of FBN1, and plan to use the CRISPR/Cas9
system to make various edits to the FBN1 gene to determine their phenotypic effects on cellular functions. After directing
Cas9 cleavage to the FBN1 gene with an appropriate guide RNA, you will utilize two different repair systems to generate
different types of FBN1 mutations.
Sort the items listed below into the repair categories provided based on their relationship to generation of FBN1 mutations
by that repair mechanism.
Introduction of a specific mutation into the FBN1 gene
Frameshift mutation
Insertion mutation
Nonhomologous end joining (NHEJ)
Repair template
Deletion mutation
Trimming off or filling in unpaired nucleotides created by a jagged double-strand DNA break
Homology-directed repair (HDR)
Transcribed Image Text:You are interested in studying the FBN1 gene, a candidate identified via GWAS for a gene involved in heritable risk of heart disease. You have a human cardiac myocyte cell line with wild type alleles of FBN1, and plan to use the CRISPR/Cas9 system to make various edits to the FBN1 gene to determine their phenotypic effects on cellular functions. After directing Cas9 cleavage to the FBN1 gene with an appropriate guide RNA, you will utilize two different repair systems to generate different types of FBN1 mutations. Sort the items listed below into the repair categories provided based on their relationship to generation of FBN1 mutations by that repair mechanism. Introduction of a specific mutation into the FBN1 gene Frameshift mutation Insertion mutation Nonhomologous end joining (NHEJ) Repair template Deletion mutation Trimming off or filling in unpaired nucleotides created by a jagged double-strand DNA break Homology-directed repair (HDR)
Expert Solution
trending now

Trending now

This is a popular solution!

steps

Step by step

Solved in 4 steps

Blurred answer
Knowledge Booster
Genomic studies
Learn more about
Need a deep-dive on the concept behind this application? Look no further. Learn more about this topic, biology and related others by exploring similar questions and additional content below.
Recommended textbooks for you
Human Anatomy & Physiology (11th Edition)
Human Anatomy & Physiology (11th Edition)
Biology
ISBN:
9780134580999
Author:
Elaine N. Marieb, Katja N. Hoehn
Publisher:
PEARSON
Biology 2e
Biology 2e
Biology
ISBN:
9781947172517
Author:
Matthew Douglas, Jung Choi, Mary Ann Clark
Publisher:
OpenStax
Anatomy & Physiology
Anatomy & Physiology
Biology
ISBN:
9781259398629
Author:
McKinley, Michael P., O'loughlin, Valerie Dean, Bidle, Theresa Stouter
Publisher:
Mcgraw Hill Education,
Molecular Biology of the Cell (Sixth Edition)
Molecular Biology of the Cell (Sixth Edition)
Biology
ISBN:
9780815344322
Author:
Bruce Alberts, Alexander D. Johnson, Julian Lewis, David Morgan, Martin Raff, Keith Roberts, Peter Walter
Publisher:
W. W. Norton & Company
Laboratory Manual For Human Anatomy & Physiology
Laboratory Manual For Human Anatomy & Physiology
Biology
ISBN:
9781260159363
Author:
Martin, Terry R., Prentice-craver, Cynthia
Publisher:
McGraw-Hill Publishing Co.
Inquiry Into Life (16th Edition)
Inquiry Into Life (16th Edition)
Biology
ISBN:
9781260231700
Author:
Sylvia S. Mader, Michael Windelspecht
Publisher:
McGraw Hill Education