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Production of CFTR-ΔF508 Rabbits

Cystic Fibrosis (CF) is a lethal autosomal recessive disease caused by mutations in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR). The most common mutation is the deletion of phenylalanine residue at position 508 (ΔF508). Here we report the production of CFTR-ΔF508...

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Autores principales: Yang, Dongshan, Liang, Xiubin, Pallas, Brooke, Hoenerhoff, Mark, Ren, Zhuoying, Han, Renzhi, Zhang, Jifeng, Chen, Y. Eugene, Jin, Jian-Ping, Sun, Fei, Xu, Jie
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7862758/
https://www.ncbi.nlm.nih.gov/pubmed/33552140
http://dx.doi.org/10.3389/fgene.2020.627666
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author Yang, Dongshan
Liang, Xiubin
Pallas, Brooke
Hoenerhoff, Mark
Ren, Zhuoying
Han, Renzhi
Zhang, Jifeng
Chen, Y. Eugene
Jin, Jian-Ping
Sun, Fei
Xu, Jie
author_facet Yang, Dongshan
Liang, Xiubin
Pallas, Brooke
Hoenerhoff, Mark
Ren, Zhuoying
Han, Renzhi
Zhang, Jifeng
Chen, Y. Eugene
Jin, Jian-Ping
Sun, Fei
Xu, Jie
author_sort Yang, Dongshan
collection PubMed
description Cystic Fibrosis (CF) is a lethal autosomal recessive disease caused by mutations in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR). The most common mutation is the deletion of phenylalanine residue at position 508 (ΔF508). Here we report the production of CFTR-ΔF508 rabbits by CRISPR/Cas9-mediated gene editing. After microinjection and embryo transfer, 77 kits were born, of which five carried the ΔF508 mutation. To confirm the germline transmission, one male ΔF508 founder was bred with two wild-type females and produced 16 F1 generation kits, of which six are heterozygous ΔF508/WT animals. Our work adds CFTR-ΔF508 rabbits to the toolbox of CF animal models for biomedical research.
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spelling pubmed-78627582021-02-06 Production of CFTR-ΔF508 Rabbits Yang, Dongshan Liang, Xiubin Pallas, Brooke Hoenerhoff, Mark Ren, Zhuoying Han, Renzhi Zhang, Jifeng Chen, Y. Eugene Jin, Jian-Ping Sun, Fei Xu, Jie Front Genet Genetics Cystic Fibrosis (CF) is a lethal autosomal recessive disease caused by mutations in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR). The most common mutation is the deletion of phenylalanine residue at position 508 (ΔF508). Here we report the production of CFTR-ΔF508 rabbits by CRISPR/Cas9-mediated gene editing. After microinjection and embryo transfer, 77 kits were born, of which five carried the ΔF508 mutation. To confirm the germline transmission, one male ΔF508 founder was bred with two wild-type females and produced 16 F1 generation kits, of which six are heterozygous ΔF508/WT animals. Our work adds CFTR-ΔF508 rabbits to the toolbox of CF animal models for biomedical research. Frontiers Media S.A. 2021-01-22 /pmc/articles/PMC7862758/ /pubmed/33552140 http://dx.doi.org/10.3389/fgene.2020.627666 Text en Copyright © 2021 Yang, Liang, Pallas, Hoenerhoff, Ren, Han, Zhang, Chen, Jin, Sun and Xu. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Genetics
Yang, Dongshan
Liang, Xiubin
Pallas, Brooke
Hoenerhoff, Mark
Ren, Zhuoying
Han, Renzhi
Zhang, Jifeng
Chen, Y. Eugene
Jin, Jian-Ping
Sun, Fei
Xu, Jie
Production of CFTR-ΔF508 Rabbits
title Production of CFTR-ΔF508 Rabbits
title_full Production of CFTR-ΔF508 Rabbits
title_fullStr Production of CFTR-ΔF508 Rabbits
title_full_unstemmed Production of CFTR-ΔF508 Rabbits
title_short Production of CFTR-ΔF508 Rabbits
title_sort production of cftr-δf508 rabbits
topic Genetics
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7862758/
https://www.ncbi.nlm.nih.gov/pubmed/33552140
http://dx.doi.org/10.3389/fgene.2020.627666
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