Zhang et al., 2013 - Assessment of hematopoietic failure due to Rpl11 deficiency in a zebrafish model of Diamond-Blackfan anemia by deep sequencing. BMC Genomics   14:896 Full text @ BMC Genomics

Fig. 1

Benzidine staining of Rpl11-deficient zebrafish embryos and the effectiveness of translational inhibition by Rpl11 MO. (A, B, C, D), O-staining shows markedly reduced numbers of hemoglobin-stained blood cells in Rpl11-knockdown embryos; (E, F), The Rpl11–egfp construct was assembled by inserting a partial sequence of Rpl11 cDNA (containing 60 bps from the 52 UTR) and the N-terminus of egfp into modified pEGFP-N1 (the ATG codon of EGFP was removed). The sequence of Rpl11 MO1 compliments 1–24 bp of Rpl11 cDNA. Embryos co-injected with 25 ng Rpl11–EGFP DNA and 0.5 ng control MO expressed EGFP, and Rpl11–EGFP expression was inhibited by co-injection with 0.5 ng Rpl11 MO; B, D, E, and F are the lateral view; A and C are the ventral view.

PHENOTYPE:
Fish:
Knockdown Reagent:
Observed In:
Stage: Long-pec

Fig. 4

Rpl11 deficiency is required for hematopoietic defects through p53-independent pathways in zebrafish embryos. A-C, Rpl11 is required for HSC formation through p53-independent pathways. The expression of cmyb was significantly decreased in Rpl11 morphants and in Rpl11 and p53 double morphants at 48 hpf compared with that in control embryos. D-I, Rpl11 deficiency caused defective hematopoietic phenotypes in zebrafish embryos through p53-independent pathways. Hemoglobin staining of embryos individually injected with Rpl11 MO or Rps19 MO and coinjected with p53 MO were performed. D and G are controls, E and H are Rpl11 MO or Rps19 knockdown, and F and I are Rpl11 MO and Rps19 MO coinjected with p53 MO, respectively. Panel AC, lateral views; D-I, ventral views.

Acknowledgments:
ZFIN wishes to thank the journal BMC Genomics for permission to reproduce figures from this article. Please note that this material may be protected by copyright. Full text @ BMC Genomics