Fig. 4
- ID
- ZDB-FIG-120209-20
- Publication
- Zhang et al., 2012 - Zebrafish Models for Dyskeratosis Congenita Reveal Critical Roles of p53 Activation Contributing to Hematopoietic Defects through RNA Processing
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Analysis of telomere maintenance and rRNA processing in zebrafish dkc1 and nola1 defeicency. (A) TRAP Assay results showed no difference between dkc1 morphants, nola1 mutants and control embryos at 3 dpf when the mutant phenotype onset (a and b). (c) We injected dkc1 MO into Tg(c-myb:GFP) fish. GFP-positive HSC were isolated by cell sorting (FACS) at 3 dpf. GFP positive (GFP+) and negative (GFP-) cells from control embryos (0 ng MO) and dkc1 morphants (15 ng MO) were subjected to TRAP Assay. IC: Internal control; -ctrl: only lysis buffer but no embryo extracts added group. (B)Analysis of RNA processing showed that reduction of 18 S rRNA in dkc1 morphant (a and b) at 48 hpf and in nola1 mutant (c and d) at 3 dpf, but slight change or no change of 28 S rRNA. The average fold changes of percentage of 18 S rRNA and 28 S rRNA are represented by the bar graphs. WT: wild type control; MO: dkc1 morphant; nola1-/-: nola1 mutant. ** indicates very significant changes at p<0.01, and * indicates significant changes at p<0.05 on the basis of independent Student t tests. |
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Stage Range: | Long-pec to Protruding-mouth |