Diamond-Blackfan anemia (DBA) is a rare inherited bone marrow failure syndrome 
that is characterized by pure red-cell aplasia and associated physical 
deformities. It has been proven that defects of ribosomal proteins can lead to 
this disease and that RPS19 is the most frequently mutated gene in DBA patients. 
Previous studies suggest that p53-dependent genes and pathways play important 
roles in RPS19-deficient embryos. However, whether there are other vital factors 
linked to DBA has not been fully clarified. In this study, we compared the whole 
genome RNA-Seq data of zebrafish embryos injected with RPS19 morpholino (RPS19 
MO), RPS19 and p53 morpholino simultaneously (RPS19+p53 MO) and control 
morpholino (control). We found that genes enriched in the functions of 
hematological systems, nervous system development and skeletal and muscular 
disorders had significant differential expression in RPS19 MO embryos compared 
with controls. Co-inhibition of p53 partially alleviates the abnormalities for 
RPS19-deficient embryos. However, the hematopoietic genes, which were 
down-regulated significantly in RPS19 MO embryos, were not completely recovered 
by the co-inhibition of p53. Furthermore, we identified the genome-wide 
p53-dependent and -independent genes and pathways. These results indicate that 
not only p53 family members but also other factors have important impacts on 
RPS19-deficient embryos. The detection of potential pathogenic genes and 
pathways provides us a new paradigm for future research on DBA, which is a 
systematic and complex hereditary disease.