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Fig. 5

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Figures for Renz et al., 2015
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Fig. 5

Blood-Flow-Independent Expression of klf2a/b mRNA in ccm2m201 Mutants

(A–C) The ccm2m201 mutant cardiac ballooning phenotype is flow independent. Frontal views of 48 hrpf hearts of the myocardial reporter line Tg(myl7:GFP)twu34 (Huang et al., 2003) show that cardiac expansion is not rescued in ccm2m201 mutant; tnnt2a morphants that lack blood flow.

(D) The expression levels of klf2a and klf2b mRNA, as measured by qRT-PCR, are elevated in ccm2m201 mutant; tnnt2a morphants that lack blood flow.

(E–G) Loss of Ccm2 results in overproliferation of the endocardium under no-flow conditions. (E) Quantifications of the ratio of proliferating versus nonproliferating endocardial cells between 33 and 53 hrpf in tnnt2a morphants compared with ccm2m201 mutant;tnnt2a morphants based on SPIM recordings (n = 2). (F) The endocardium of tnnt2a morphants is not proliferative as indicated by the lack of color-coded proliferative cells (still image derived from Movie S1, which is based on SPIM time-lapse recordings of endocardial morphogenesis marked by Tg(kdrl:GFP)s843 between 33 and53 hrpf). (G) The combined loss of Ccm2 and Tnnt2a is characterized by a high rate of proliferative events (indicated by uniquely colored daughter cells derived from proliferative events; still image derived from Movie S2). A, atrium; V, ventricle. Statistical data are means and SEM; ns, not significant; p < 0.05; p < 0.01; p < 0.001; p < 0.0001; see  Supplemental Experimental Procedures for details about statistical data analysis.

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Reprinted from Developmental Cell, 32, Renz, M., Otten, C., Faurobert, E., Rudolph, F., Zhu, Y., Boulday, G., Duchene, J., Mickoleit, M., Dietrich, A.C., Ramspacher, C., Steed, E., Manet-Dupé, S., Benz, A., Hassel, D., Vermot, J., Huisken, J., Tournier-Lasserve, E., Felbor, U., Sure, U., Albiges-Rizo, C., Abdelilah-Seyfried, S., Regulation of β1 Integrin-Klf2-Mediated Angiogenesis by CCM Proteins, 181-190, Copyright (2015) with permission from Elsevier. Full text @ Dev. Cell