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. 2000 Oct 30;151(3):563–572. doi: 10.1083/jcb.151.3.563

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© 2000 The Rockefeller University Press

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).

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Expression of the β-galactosidase gene (Krt1-19-lacZ) in the heterozygous mouse embryos at 7.5–9.0 dpc. (a and b) A representative embryo at 7.5 dpc in the anterior and posterior views, respectively. Note the β-galactosidase activity in the notochordal plate, node, and ectoplacental cone. (c) A representative embryo at 8.5 dpc in the posterior view. Note the β-galactosidase activity in an arch pattern (arrows). (d and e) Another embryo at 8.5 dpc in the anterior (d) and posterior (e) views. Note that this embryo is more progressed in development than that in c: the arch pattern of the β-galactosidase staining at the hindgut (e, arrows) is much smaller than that seen in the embryo shown in c. Also note the staining inside the foregut in d (arrow). (f and g) A representative embryo at 9.0 dpc. (h) A transverse section of the same embryo shown in f and g (Eosin counterstaining). hf, head fold; nc, notochordal plate; nd, node; pg, primitive gut. All dissection micrographs (whole mount in situ staining) were taken under a dark-field illumination, except a and g, which were in a bright field. Bar, 100 μm.