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Reduction of XNkx2-10 expression leads to anterior defects and malformation of the embryonic heart
Journal article   Open access   Peer reviewed

Reduction of XNkx2-10 expression leads to anterior defects and malformation of the embryonic heart

Bryan G Allen, Kristina Allen-Brady and Daniel L Weeks
Mechanisms of development, Vol.123(10), pp.719-729
2006
DOI: 10.1016/j.mod.2006.07.008
PMCID: PMC2094041
PMID: 16949797
url
https://doi.org/10.1016/j.mod.2006.07.008View
Published (Version of record) Open Access

Abstract

Normal vertebrate heart development depends upon the expression of homeodomain containing proteins related to the Drosophila gene, tinman. In Xenopus laevis, three such genes have been identified in regions that will eventually give rise to the heart, XNkx2-3, XNkx2-5 and XNkx2-10. Although the expression domains of all three overlap in early development, distinctive differences have been noted. By the time the heart tube forms, there is little XNkx2-10 mRNA detected by in situ analysis in the embryonic heart while both XNkx2-3 and XNkx2-5 are clearly present. In addition, unlike XNkx2-3 and XNkx2-5, injection of XNkx2-10 mRNA does not increase the size of the embryonic heart. We have reexamined the expression and potential role of XNkx2-10 in development via oligonucleotide-mediated reduction of XNkx2-10 protein expression. We find that a decrease in XNkx2-10 leads to a broad spectrum of developmental abnormalities including a reduction in heart size. We conclude that XNkx2-10, like XNkx2-3 and XNkx2-5, is necessary for normal Xenopus heart development.
Nkx tinman Congenital defects Xenopus heart development

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