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myl2xenopus   

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Experiment details for myl2

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.

Gene Clone Species Stages Anatomy
myl2.S laevis NF stage 35 and 36 heart , myocardium , endocardium

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  Fig.5. Lurp1 morpholino affects myeloid domain migration and cardiac muscle morphogenesis. (A–H) A stage 25 embryo injected with the lurp1-MO into both blastomeres at the two-cell stage (2/2) (A and B), 12 ng dose. Embryos similarly injected into dorsal blastomeres (C and D), or as a control in ventral blastomeres (E and F), or non-injected sibling (G and H) and hybridized with probes for mpo and nkx2-5. (I–P) Stage 35 tadpoles injected with the lurp1 morpholino, 12 ng dose, with the same sequence of blastomere injections presented and hybridized to mpo and mlc2. Anterior is to the left in lateral and detail ventral views. (Q–S) Transverse section through the heart region of tadpoles injected with lurp1 morpholino. Examples of a cardiac bifida phenotype (I, J, Q) and abnormal myocardial folding morphogenesis (K, L, R) were observed in both the two-cell stage and dorsal blastomere injection experiments but never after ventral blastomere injection (M, N, S). (T and U) Stage 25 heart field sections of embryo with dorsal blastomere morpholino (C, D, T) and non-injected sibling (G, H, U). Green arrowheads show dark mpo stain of macrophages. Asterisk (*) denotes mesodermal nkx2-5 stain. NFR-counterstained. Scale bar = 100 μm. Sp, section plane; M, myeloid/macrophage; En, endoderm; Mc, myocardium; Ec, endocardium.