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Fig. 6
CM proliferation is inversely regulated by Smad2 and Smad3. a Experimental setup of SIS3 treatment, followed by EdU treatment and fixation. b, c Tg(myl7:nlsDsRedExpress) hearts of untreated control and 3?µM SIS3-treated larvae at 120 hpf; ?-DsRed (red), EdU (green). White arrowheads point to proliferating CMs (EdU+/DsRed+). d Quantification of CM proliferation in untreated control (n?=?4) and 3?µM SIS3-treated (n?=?5) ventricles at 120 hpf. e Experimental setup of injections, followed by EdU treatment and fixation. f?i Tg(myl7:nlsDsRedExpress) hearts of myl7:H2B-EGFP, myl7:H2B-EGFP-2A-caSmad2, myl7:H2B-EGFP-2A-caSmad3a and myl7:H2B-EGFP-2A-caSmad3b injected larvae at 120 hpf; ?-DsRed (red), ?-GFP (blue), EdU (green). White arrowheads point to proliferating CMs (EdU+/DsRed+/GFP +). j Quantification of CM proliferation in myl7:H2B-EGFP (n?=?10), caSmad2 (n?=?10), caSmad3a (n?=?10), and caSmad3b (n?=?10) injected ventricles at 120 hpf. All cell counts were performed on non-overlapping confocal planes (thickness, 1?µm) (data are mean?±?s.e.m., *P???0.05 and ***P???0.001?Student?s t test, two-tailed). Scale bars, 20?µm. vent., ventricle; atr., atrium