Supplementary information

Development 143: doi:10.1242/dev.130534: Supplementary information
Supplementary Figure S1. In situ hybridization for selected genes. In situ hybridization for
STOP-loxP-DTA animals treated with tamoxifen) and injured hearts (ventricles at 7 dpi
cmlc2:CreER; bactin2:loxP-mCherry-STOP-loxP-DTA animals treated with tamoxifen).
in
Development • Supplementary information
selected genes was performed on sections of uninjured hearts (ventricles from bactin2:loxP-mCherry-
Supplementary Figure S2. In situ hybridization on embryos. In situ hybridization for selected
genes was performed using 3 dpf or 4 dpf embryos.
Development • Supplementary information
Development 143: doi:10.1242/dev.130534: Supplementary information
Development • Supplementary information
Development 143: doi:10.1242/dev.130534: Supplementary information
Development • Supplementary information
Development 143: doi:10.1242/dev.130534: Supplementary information
Development • Supplementary information
Development 143: doi:10.1242/dev.130534: Supplementary information
Development 143: doi:10.1242/dev.130534: Supplementary information
Supplementary Figure S3. Representative sections from each of 91 hearts of wild-types (A), cav1
heterozygotes (B), and cav1 homozygotes (C), at 30 dpa. Sections from uninjured cav1 homozygous
mutant hearts are shown in (D). Ventricular sections are stained for MHC (green) to denote cardiac
muscle. The same sections in left panels are stained with acid fuchsin orange G to characterize non-
Development • Supplementary information
muscle components in the injuries (right; blue for collagen, red for fibrin).
Development 143: doi:10.1242/dev.130534: Supplementary information
Supplementary Figure S4. A second allele of cav1 disrupts heart regeneration. (A) The TALEN
pairs were used to target to the sequences labeled in red, which is the common sequence of both
isoforms. A mutant with a 23-nt deletion, cav1pd1104, was identified, which leads to truncated proteins
of both a and b isoforms lacking all the important domains for caveolae formation. (B) cav1pd1104
heterozygous mutants (right) displayed severe defects in muscle regeneration (top) and fibrin/collagen
muscle. Dashed line indicates plane of resection. The same sections in top panels are stained with
acid fuchsin orange G to characterize non-muscle components in the injuries (bottom; blue for
collagen, red for fibrin). (C) Quantification of regeneration scores between cav1 mutants and wildtype siblings were compared at 30 dpa. Data indicate the percent of total hearts represented by each
score for each genotype. n = 9 for wild-types, and n = 16 for heterozygotes.
Development • Supplementary information
retention (bottom). Section images of ventricles at 30 dpa are stained for MHC to denote cardiac
Development 143: doi:10.1242/dev.130534: Supplementary information
Supplementary Table S1. The expression (log2) of selected genes in clustered orders.
Click here to Download Table S1
Supplementary Table S2. Primers used to generate in situ hybridization probes.
Development • Supplementary information
Click here to Download Table S2