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Fig. 1
The anaemia associated with Rps19 deficiency has a Tp53 independent component. [A] rps19 knockdown was performed in both Tp53 wildtype (top panels) and Tp53 mutant (bottom panels) zebrafish lines. Staining for haemoglobin shows a profound reduction in circulating blood regardless of Tp53 status. Developmental defects associated with Rps19 deficiency were markedly improved in Tp53 mutant embryos (ii), however only modest improvements in haemoglobinization were observed. Co-injection of rps19 RNA rescued the anaemia in 50-80% of embryos regardless of Tp53 status (iii). [B] rps19 morpholino (MO) was co-injected with tp53 MO or control MO into Tg(gata1:dsRed2) transgenic embryos (upper panel shows epiflourescent image of a control embryo) at 2 days post-fertilization. Embryos were dissociated and the percentage of erythroid cells (dsRed2 expressing) determined by fluorescence-activated cell sorting. A significant reduction in dsRed2 expressing cells in Rps19 morphants compared to controls was observed. The addition of Tp53 MO partially rescued red cell numbers but did not show an overall improvement in total red cell numbers compared to Rps19 knockdown in the presence of control MO, indicating a Tp53 independent component to the anaemia observed in the Rps19 morphants.