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. Author manuscript; available in PMC: 2015 Nov 1.
Published in final edited form as: Nat Genet. 2015 Mar 25;47(5):496–504. doi: 10.1038/ng.3250

Fig. 2. Deletion of Gata4 in the PPFs produces localized amuscular regions that are weaker than juxtaposed muscular regions and results in CDH.

Fig. 2

(a–d) CDH develops in mice with Gata4 null PPF cells (n > 33/33; Bochdalek hernias labeled with white and yellow asterisks and Morgagni hernia labeled with red asterisk in b), but not in Gata4 heterozygotes (n > 66/66; a), mice with Gata4 null muscle (n = 28/28; c), or mice with muscleless diaphragms (n > 10/10; d). (e, j) Loss of muscle in diaphragms with Gata4 null PPF cells rescues herniation, indicating that juxtaposition of amuscular with muscular regions is required for CDH (n = 3/3). (g–h) In herniated regions PPF cells are present, but muscle is not (n = 7/7). (k–m), Finite element modeling shows that a hernia only develops when the amuscular region is more compliant than the muscular region. Models are lateral views (c, f–j) Whole-mount β-galactosidase staining. (a–j) Dorsal is at top. Scale bar = 1 mm (a–g, i–j), 0.5 mm (h).