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Fig. 6
Inhibition of Fgfr signaling can lead to cardiomyocyte extrusion in WT animals.
(A–D) Confocal images of 96 hpf hearts; WT animals treated with DMSO as a control or FGFR inhibitor (SU5402) from 75 to 96 hpf; maximum intensity projections of hearts in (A) and (D) are shown in (C) and (D) respectively; arrows point to extruding cardiomyocytes. (E–H) 75 hpf Tg(myl7: mCherry-CAAX) (E–F) or Tg(hsp70:dn-fgfr1-EGFP);Tg(myl7: mCherry-CAAX) (G–H) animals were heat-stressed at 39°C for 1 hr (F and H) and their hearts imaged at 96 hpf; arrow in (H) points to an extruding cardiomyocyte (n = 9/13 hearts). (I) klf2a+/-; klf2b-/- animals are more likely than WT siblings to exhibit cardiomyocyte extrusion upon Fgfr inhibition; number of treated larvae for each condition is shown above the individual columns. (J–K) Hearts of 96 hpf Tg(myl7: mCherry-CAAX); klf2 +/+ or klf2 -/- animals immunostained for pERK. (L–M) Hearts of 96 hpf Tg(fli1a:klf2b-p2A-tdTomato);Tg(myl7:EGFP-Hsa.HRAS); klf2 +/+ or klf2 -/- animals immunostained for pERK. Arrows and arrowheads point to extruding cardiomyocytes and pERK positive endocardial cells, respectively; V: ventricle, At: atrium; scale bars, 50 µm.