Open AccessLeft‐right lineage analysis of AV cushion tissue in normal and laterality defective Xenopus hearts
Author(s) -
Ramsdell Ann F.,
Bernanke Jayne M.,
Johnson John,
Trusk Thomas C.
Publication year - 2005
Publication title -
the anatomical record part a: discoveries in molecular, cellular, and evolutionary biology
Language(s) - English
Resource type - Journals
eISSN - 1552-4892
pISSN - 1552-4884
DOI - 10.1002/ar.a.20269
Subject(s) - xenopus , laterality , biology , anatomy , lineage (genetic) , atrioventricular canal , atrioventricular cushions , population , embryo , microbiology and biotechnology , medicine , heart disease , genetics , neuroscience , environmental health , gene
The majority of complex congenital heart defects occur in individuals who are afflicted by laterality disease. We hypothesize that the prevalence of valvuloseptal defects in this population is due to defective left‐right patterning of the embryonic atrioventricular (AV) canal cushions, which are the progenitor tissue for valve and septal structures in the mature heart. Using embryos of the frog Xenopus laevis , this hypothesis was tested by performing left‐right lineage analysis of myocytes and cushion mesenchyme cells of the superior and inferior cushion regions of the AV canal. Lineage analyses were conducted in both wild‐type and laterality mutant embryos experimentally induced by misexpression of ALK4, a type I TGF‐β receptor previously shown to modulate left‐right axis determination in Xenopus. We find that abnormalities in overall amount and left‐right cell lineage composition are present in a majority of ALK4‐induced laterality mutant embryos and that much variation in the nature of these abnormalities exists in embryos that exhibit the same overall body situs. We propose that these two parameters of cushion tissue formation—amount and left‐right lineage origin—are important for normal processes of valvuloseptal morphogenesis and that defective allocation of cells in the AV canal might be causatively linked to the high incidence of valvuloseptal defects associated with laterality disease. © 2005 Wiley‐Liss, Inc.