p53 loss but not overexpression of bcl-xl rescues development and myeloid defects in ddx18^{hi1727/hi1727} mutants. (A-F) Lateral views, head to the left, dorsal upwards of 27-hpf embryos. (A,C,E) ddx18^hi1727 siblings and (B,D,F) ddx18^hi1727 homozygous mutants injected with control (mcherry-encoding [100 pg] RNA; A-B), p53 morpholino (1.6 ng; C-D), or Bcl-xl–encoding RNA (100 pg; E-F). Embryos are stained using 2-color WISH for mpx in black and ddx18 in red. ddx18^{hi1727/hi1727} were identified by the absence of expression of ddx18. Arrowheads denote ddx18 expression in the eye and forebrain of sibling embryos which is absent in mutant embryos. Injection of p53 morpholino but not bcl-xl RNA was able to completely rescue both developmental and myeloid defects observed at 27 hpf. (G) Scatter plot quantifying number of mpx⁺ cells per embryo. ***P < .0005 unpaired Student t test. (H-I) mCherry(H) and bcl-xl (I) RNA-injected embryos were irradiated with 12 Gy at 24 hpf and stained using the supravital dye acridine orange 6 hours postirradiation (HPI) to detect cell death. bcl-xl–injected embryos were resistant to irradiation-induced cell death indicating functional Bcl-xl protein is translated in vivo. Epifluorescent images were acquired on a Nikon SMZ1500 zoom stereomicroscope (Nikon Instruments Inc) using a 488-nm filter. ns indicates not significant.