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Early embryonic expression of AP-2a is critical for cardiovascular development

Lookup NU author(s): Amy-Leigh Johnson, Professor Deborah HendersonORCiD, Dr Helen PhillipsORCiD, Dr Simon BamforthORCiD

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This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).


Abstract

Congenital cardiovascular malformation is a common birth defect and incorporates abnormalities of the outflow tract and aortic arch arteries. Mice deficient for the transcription factor AP-2a (Tcfap2a) have complex outflow tract and arch artery malformations. AP-2a is expressed in the pharyngeal surface ectoderm and neural crest at mid-embryogenesis, but the precise tissue compartment in which AP-2a is required for cardiovascular development has not been identified. In this study we describe the fully penetrant AP-2a deficient cardiovascular phenotype on a C57Bl/6J genetic background and show that this is associated with increased apoptosis in the pharyngeal ectoderm. Neural crest cell migration into the pharyngeal arches was not affected. Using Cre expressing transgenic mice in conjunction with an AP-2a conditional allele to examine the effect of deleting AP-2a from the pharyngeal surface ectoderm, the neural crest and the second heart field was, surprisingly, unable to recapitulate the global AP-2a deficient cardiovascular phenotype. The outflow tract and arch artery phenotype was, however, recapitulated through early embryonic Cre-mediated recombination.


Publication metadata

Author(s): Johnson A-L, Schneider JE, Mohun TJ, Williams T, Bhattacharya S, Henderson DJ, Phillips HM, Bamforth SD

Publication type: Article

Publication status: Published

Journal: Journal of Cardiovascular Development and Disease

Year: 2020

Volume: 7

Issue: 3

Online publication date: 23/07/2020

Acceptance date: 22/07/2020

Date deposited: 27/07/2020

ISSN (electronic): 2308-3425

Publisher: MDPI AG

URL: https://doi.org/10.3390/jcdd7030027

DOI: 10.3390/jcdd7030027


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Funding

Funder referenceFunder name
2R01 DE12728
FS/08/016/24741British Heart Foundation
FS/09/015/26934British Heart Foundation
SI/14/1/30718

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