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XB-IMG-175407

Xenbase Image ID: 175407


FIGURE 1 Light induction of tadpoles with KillerRed expression in the heart induces transient ventricular hypertrophy and cardiomyocyte proliferation. (a) The ventricle of KillerRed‐expressing/light activated tadpoles (Treated) is enlarged at 9 hr relative to sibling control hearts. Immunohistochemistry for cardiac troponin T (CT3). Scale bar = 100 μm. (b) (i) The volume of KillerRed‐expressing tadpole ventricles exposed to green light (Treated), normalized to uninjected stage‐matched sibling controls (Control), increases significantly over that of control ventricles in a period between 9 and 24 hr after removal from light. n = 35–162 tadpoles, N = 2–6 replicates. (ii) Ventricular volume increases significantly in treated tadpoles over controls at 3 and 5 days post‐light exposure. n = 19–60 tadpoles, N = 1–3 replicates. (c) The number of proliferating cells in the ventricular myocardium in KillerRed‐expressing/light activated tadpoles (Treated) increases at 4 days relative to sibling control hearts. Histone H3 p‐Ser10 (H3P) positive loci were used to mark proliferating nuclei, and cardiac troponin T (CT3) was used to determine whether proliferating cells were cardiomyocytes. H3P+ cells were counted within a randomly selected region in the ventricle (inset). Scale bar = 100 μm. (d) (i) There is no change in cardiomyocyte proliferation in KillerRed‐expressing hearts exposed to light, as measured by density of H3P+ positive loci in the ventricle, relative to control hearts in the first 24 hr after light exposure. n = 15–49 tadpoles, N = 1–2 replicates. (ii) Proliferation increases significantly in KillerRed‐expressing and light‐activated tadpole hearts over uninjected stage‐matched sibling controls at two time points, 4 and 7 days post‐light exposure. n = 11–38 tadpoles, N = 1–2 replicates. *p < 0.05; **p < 0.01 (t‐t e s t w i t h H o l m c o r r e c t i o n ) . □ C o n t r o l ,Treated

Image published in: Jewhurst K and McLaughlin KA (2019)

Copyright © 2019. Image reproduced with permission of the Publisher, John Wiley & Sons.

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