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. Author manuscript; available in PMC: 2014 Feb 25.
Published in final edited form as: Dev Cell. 2013 Feb 25;24(4):411–425. doi: 10.1016/j.devcel.2013.01.018

Figure 5. Rpl22 and Rpl22l1 are unable to cross-compensate defects caused by loss of their paralog.

Figure 5

(A–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 co-injected with the indicated heat-inducible rescue plasmids. Expression of Rpl22/Rpl22l1 was restored by heating for 1h at 37°C at either 3dpf (A) or 12hpf (B) following which effects on T cell development were assessed by WISH at 5dpf with an lck probe (A) and effects on HSC emergence were assessed at 24hpf using a runx1 probe. Thymocytes (A; red dashed rectangles). HSC (B; red arrowheads).

Images depict phenotypes representative of at least 3 separate experiments, with numbers referring to the fraction of morphants with the depicted phenotypes. See also Figures S5.