A CRISPR/Cas9‐engineered mouse carrying a conditional knockout allele for the early growth response‐1 transcription factor

Author:

Maurya Vineet K.1ORCID,Ying Yan1ORCID,Lanza Denise G.2ORCID,Heaney Jason D.2ORCID,Lydon John P.1ORCID

Affiliation:

1. Department of Molecular and Cellular Biology Baylor College of Medicine One Baylor Plaza Houston Texas 77030 USA

2. Department of Molecular and Human Genetics Baylor College of Medicine One Baylor Plaza Houston Texas 77030 USA

Abstract

SummaryEarly growth response 1 (EGR1) mediates transcriptional programs that are indispensable for cell division, differentiation, and apoptosis in numerous physiologies and pathophysiologies. Whole‐body EGR1 knockouts in mice (Egr1KO) have advanced our understanding of EGR1 function in an in vivo context. To extend the utility of the mouse to investigate EGR1 responses in a tissue‐ and/or cell‐type‐specific manner, we generated a mouse model in which exon 2 of the mouse Egr1 gene is floxed by CRISPR/Cas9 engineering. The floxed Egr1 alleles (Egr1f/f) are designed to enable spatiotemporal control of Cre‐mediated EGR1 ablation in the mouse. To confirm that the Egr1f/f alleles can be abrogated using a Cre driver, we crossed the Egr1f/f mouse with a global Cre driver to generate the Egr1 conditional knockout (Egr1d/d) mouse in which EGR1 expression is ablated in all tissues. Genetic and protein analysis confirmed the absence of exon 2 and loss of EGR1 expression in the Egr1d/d mouse, respectively. Moreover, the Egr1d/d female exhibits overt reproductive phenotypes previously reported for the Egr1KO mouse. Therefore, studies described in this short technical report underscore the potential utility of the murine Egr1 floxed allele to further resolve EGR1 function at a tissue‐ and/or cell‐type‐specific level.

Funder

National Institute of Child Health and Human Development

National Institutes of Health

Publisher

Wiley

Subject

Cell Biology,Endocrinology,Genetics

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3