Neuromics' Islet-1 Used to Study Avian Heart Morphology

Evolution of High-Performance Hearts

Our Islet-1 Antibody showed its versatility a comparative morphology of avian hearts.

Figure: Sinuatrial node in Mallard (a–c), chicken HH42 (d–g), Lesser redpoll (h–j), and Jackdaw (k–m). All sections are in the transverse plane. The boxed areas in the left-hand column images indicate the areas of the images of the middle and right-hand columns. (a–c) In the Mallard, a nodal structure at the base of the right leaflet of the sinuatrial valve (black arrowhead in [a]) expressed Isl1 (b, c) and had a large coronary artery (white arrowhead in [b]). Sections 271 (cranial) to 1201 (caudal) encompassed the atria and the sections shown are 691 (a), 692 (b), 762 (c). (d–g) In the chicken HH42, the sinus venosus (SV) expressed the myocardial marker cTnI and this expression was relatively weak at the base of the right leaflet of the sinuatrial valve (black arrowhead in [e]). (f–g) The base of the right leaflet of the sinuatrial valve expressed Bmp2 (red arrowheads in [f]) and Isl1 [g]). Sections 17 (cranial) to 297 (caudal) encompassed the atria and the sections shown are 80 (d-e), 78 (f ), 88 (g). The sections were from the mid-height of the atria. (h–j) In the lesser redpoll, Isl1 was expressed in the base of the right leaflet of the sinuatrial valve. There was no nodal structure but the Isl1 expressing wall was thicker than the surrounding walls and contained a large coronary artery (white arrowhead in [i]). Sections 321 (cranial) to 621 (caudal) encompassed the atria and the sections shown are 401 (h), 402 (i), 422 (j). (k–m) In the Jackdaw an Isl1 positive area was seen in the left sinus venosus myocardium (l) in which a coronary artery was visible (white arrowhead in (l). At the base of the right sinuatrial leaflet no positive Isl1 cells could be seen (m). Sections 122 (cranial) to 332 (caudal) encompassed the atria and the sections shown are 190 (k) and 191 (l–m). Ao = aorta; LA = left atrium; PA = pulmonary artery; RA = right atrium; SAJ = sinuatrial junction. In the picro-sirius red images blood has been painted over with white for clarity. DOI: 10.1002/jmor.20952

We have an extensive catalog of high-performance antibodies.

Molecular Pathways and Heart Development

Owen WJ Prall, Mary K Menon, Mark J Solloway, Yusuke Watanabe, Stéphane Zaffran, Fanny Bajolle, Christine Biben, Jim J McBride, Bronwyn R Robertson, Hervé Chaulet, Fiona A Stennard, Natalie Wise, Daniel Schaft, Orit Wolstein, Milena B Furtado, Hidetaka Shiratori,6 Kenneth R Chien, Hiroshi Hamada,6 Brian L Black, Yumiko Saga, Elizabeth J Robertson, Margaret E Buckingham, and Richard P Harvey. An Nkx2-5/Bmp2/Smad1 negative feedback loop controls second heart field progenitor specification and proliferation. Cell. 2007 March 9; 128(5): 947–959. doi: 10.1016/j.cell.2007.01.042.

Summary: During heart development the second heart field (SHF) provides progenitor cells for most cardiomyocytes and expresses the homeodomain factor Nkx2-5. We now show that feedback repression of Bmp2/Smad1 signaling by Nkx2-5 critically regulates SHF proliferation and outflow tract (OFT) morphology. In the cardiac fields of Nkx2-5 mutants, genes controlling cardiac specification (including Bmp2) and maintenance of the progenitor state were up-regulated, leading initially to progenitor over-specification, but subsequently to failed SHF proliferation and OFT truncation. In Smad1 mutants, SHF proliferation and deployment to the OFT were increased, while Smad1 deletion in Nkx2-5 mutants rescued SHF proliferation and OFT development. In Nkx2-5 hypomorphic mice, which recapitulate human congenital heart disease (CHD), OFT anomalies were also rescued by Smad1 deletion. Our findings demonstrate that Nkx2-5 orchestrates the transition between periods of cardiac induction, progenitor proliferation and OFT morphogenesis via a Smad1-dependent negative feedback loop, which may be a frequent molecular target in CHD.

...goat anti-Isl1, raised against full length human Isl1, GT15051, Neuromics)...