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Fig. S3
The hematopoietic defects of rpc9-/- mutants are independent of calcitonin signaling pathway. (A) Confocal imaging showed that Rpc9-EGFP fusion protein was enriched in the nucleus rather than the membrane of embryonic zebrafish cells at 9 hpf. (B) Western blot assay confirmed Rpc9 in the nucleus. β-Tubulin, cytoplasmic proteinmarker. LaminB1, nuclear proteinmarker. (C) The cAMP level of rpc9-/- embryos was slightly lower than that of rpc9+/+ embryos (mean±SD, *P < 0.05). (D) The absence of rag1 in the thymus of rpc9-/- embryos was not rescued by Forskolin administration. (E) 8-Bromo-cAMP treatment could not restore the T cell defects in rpc9-/- mutants. (F) MK-3207 treatment led to a significant decrease of cAMP level (mean±SD, *** < P0.001). (G) Embryos treated with MK-3207 showed no obvious T cell or HSPC defects. Note that arrowheads in (D), (E) and (G) mark the thymus or the CHT.