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Ribosomes are responsible for protein synthesis in all cells. Ribosomal protein S19 (RPS19) is one of the 79 ribosomal proteins (RPs) in vertebrates. Heterozygous mutations in  RPS19  have been identified in 25% of patients with Diamond-Blackfan anemia (DBA), but the relationship between  RPS19  mutations and the pure red-cell aplasia of DBA is unclear. In this study, we developed an RPS19-deficient zebrafish by knocking down  rps19  using a Morpholino antisense oligo. The RPS19-deficient animals showed a dramatic decrease in blood cells as well as deformities in the head and tail regions at early developmental stages. These phenotypes were rescued by injection of zebrafish  rps19  mRNA, but not by injection of  rps19  mRNAs with mutations that have been identified in DBA patients. Our results indicate that  rps19  is essential for hematopoietic differentiation during early embryogenesis. The effects were specific to  rps19 , but knocking down the genes for three other RPs,  rpl35, rpl35a  and  rplp2 , produced similar phenotypes, suggesting that these genes might have a common function in zebrafish erythropoiesis. The RPS19-deficient zebrafish will provide a valuable tool for investigating the molecular mechanisms of DBA development in humans.

Deficiency of ribosomal protein S19 during early embryogenesis leads to reduction of erythrocytes in a zebrafish model of Diamond-Blackfan anemia