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Lookup NU author(s): Amy-Leigh Johnson, Professor Deborah HendersonORCiD, Dr Helen PhillipsORCiD, Dr Simon BamforthORCiD
This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).
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.
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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