FIGURE

Fig. 5

ID

ZDB-FIG-130409-12

Publication

Zhang et al., 2013 - Control of hematopoietic stem cell emergence by antagonistic functions of ribosomal protein paralogs

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Fig. 5

Rpl22 and Rpl22l1 Are Unable to Cross-Compensate Defects Caused by Loss of Their Paralog (A and B) Cross-complementation analysis of the hematopoietic defects caused by knockdown of Rpl22 and Rpl22l1. Embryos injected with Rpl22 MO, Rpl22l1 MO, or MM control were coinjected with the indicated heat-inducible rescue plasmids. Expression of Rpl22/Rpl22l1 was restored by heating for 1 hr at 37°C at either 3 dpf (A) or 12 hpf (B) after which effects on T cell development were assessed by WISH at 5 dpf with an lck probe (A) and effects on HSC emergence were assessed at 24 hpf using a runx1 probe. Thymocytes (A; red dashed rectangles). HSC (B; red arrowheads). Images depict phenotypes representative of at least three separate experiments, with numbers referring to the fraction of morphants with the depicted phenotypes. See also Figures S5.

Expression Data

Genes:	lck runx1
Fish:	WT WT + MO1-rpl22l1
Knockdown Reagent:	MO1-rpl22l1
Anatomical Terms:	hematopoietic multipotent progenitor cell T cell
Stage Range:	Prim-5 to Day 5

Expression Detail

Antibody Labeling

Phenotype Data

Phenotype Detail

Acknowledgments

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Reprinted from Developmental Cell, 24(4), Zhang, Y., Duc, A.C., Rao, S., Sun, X.L., Bilbee, A.N., Rhodes, M., Li, Q., Kappes, D.J., Rhodes, J., and Wiest, D.L., Control of hematopoietic stem cell emergence by antagonistic functions of ribosomal protein paralogs, 411-425, Copyright (2013) with permission from Elsevier. Full text @ Dev. Cell