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smad3xenopus pronephric kidney 

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Experiment details for smad3

Early cardiac morphogenesis defects caused by loss of embryonic macrophage function in Xenopus.

Early cardiac morphogenesis defects caused by loss of embryonic macrophage function in Xenopus.

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Gene Clone Species Stages Anatomy
smad3.L laevis NF stage 32 pronephric kidney

  Fig.7. Endocardial smad3 expression is detected in macrophage-morpholino defective embryos. (A–F) Tadpoles injected into dorsal blastomeres with spib morpholino, 40 ng dose (A and B), or lurp1 morpholino, 12 ng dose (C and D), or non-injected sibling (E and F). The spib morpholino caused a mild macrophage deficit phenotype (A and B) while the lurp1 morpholino induced abnormal, broadened morphology at the ventral midline (D). Tadpoles carry the Tg[smad3-egfp] reporter and were hybridized with probes for mpo and eGFP. At stage 32, the transgenic line gives eGFP expression within head, eye, pronephros, somite and notochord domains (A, C, E), while strong expression occurs in the forming endocardium, but not in myocardium at these stages, nor in macrophages. Anterior is to left in lateral views and ventral view of heart-forming regions. (G–I) Transverse heart sections of the tadpoles. Cells underlying the malformed myocardium gave endocardium-type smad3 reporter expression in morpholino tadpoles (G and H) while the forming endocardium stained strongly positive in the control (I). The right-sided myocardial region only, was presented for the morpholino injected tadpoles due to their broader ventral surface and to allow the necessary image magnification. NFR-counterstained. Scale bars = 100 μm. Sp, section plane; R, right; Mc, myocardium; Ec, endocardial cell activity.
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