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XB-ART-43170
Mech Dev. May 1, 2011; 128 (5-6): 303-15.

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



Abstract
The heart-forming mesoderm in Xenopus embryos lies adjacent to the source of the first embryonic population of macrophages. Such macrophages underlie the bilateral myocardial cell layers as they converge to form a linear heart tube. We have examined whether such macrophages participate in early cardiac morphogenesis, combining morpholino oligonucleotides that inhibit macrophage differentiation or function with transgenic reporters to assess macrophage numbers in living embryos. We show that loss of macrophage production through tadpole stages of development by morpholino-mediated knockdown of the spib transcription factor results in an arrest of heart formation. The myocardium fails to form the fused, wedge-shaped trough that precedes heart tube formation and in the most severe cases, myocardial differentiation is also impaired. Knockdown of the Ly6 protein lurp1, an early, secreted product from differentiated macrophages, produces a similar arrest to myocardial morphogenesis. Heart development can moreover be rescued by surgical-transfer of normal macrophage domains into morpholino-injected embryos. Together, these results demonstrate that amphibian heart formation depends on the presence and activity of the macrophage population, indicating that these cells may be an important source of growth cues necessary for early cardiac morphogenesis.

PubMed ID: 21515365
PMC ID: PMC3157588
Article link: Mech Dev.
Grant support: U117562103 Medical Research Council

Genes referenced: mpo myl2 nkx2-5 nucb1 slurp1l smad3 spib tbx5 tnni3
Antibodies referenced:
Morpholinos referenced: slurp1l MO1 slurp1l MO2 slurp1l MO3 spib MO2 spib MO4
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