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Heart development in fibronectin-null mice is governed by a genetic modifier on chromosome four
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Biochemistry and Microbiology.
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2007 (English)In: Mechanisms of Development, ISSN 0925-4773, E-ISSN 1872-6356, Vol. 124, no 7-8, 551-558 p.Article in journal (Refereed) Published
Abstract [en]

Absence of the fibronectin (FN) gene leads to early embryonic lethality in both 129S4 and C57BL/6J strains due to severe cardiovascular defects. However, heart development is arrested at different stages in these embryos depending on the genetic background. In the majority of 129S4 FN-null embryos, heart progenitors remain at their anterior bilateral positions and fail to fuse at the midline to form a heart tube. However, on the C57BL/6J genetic background, cardiac development progresses further and results in a centrally positioned and looped heart. To find factor(s) involved in embryonic heart formation and governing the extent of heart development in FN-null embryos in 129S4 and C57BL/6J strains, we performed genetic mapping and haplotype analyses. These analyses lead to identification of a significant linkage to a 1-Mbp interval on chromosome four. Microarray analysis and sequencing identified 21 genes in this region, including five that are differentially expressed between the strains, as potential modifiers. Since none of these genes was previously known to play a role in heart development, one or more of them is likely to be a novel modifier affecting cardiac development. Identification of the modifier would significantly enhance our understanding of the molecular underpinning of heart development and disease.

Place, publisher, year, edition, pages
2007. Vol. 124, no 7-8, 551-558 p.
National Category
Medical and Health Sciences
URN: urn:nbn:se:uu:diva-159674DOI: 10.1016/j.mod.2007.05.004PubMedID: 17628448OAI: oai:DiVA.org:uu-159674DiVA: diva2:446158
Available from: 2011-10-06 Created: 2011-10-06 Last updated: 2011-10-13Bibliographically approved

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Lindblad-Toh, Kerstin
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