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Fig. 7 Loss-of-function experiments in the zebrafish confirm the essential role of the characteristic ECM component Dcn for HSPC development. (A) WISH for runx1 in 30 hpf dcn morphants (MOSTART) and their respective uninjected controls. Right panel indicates the numbers of runx1+ cells in the dorsal aorta of control and dcn morphant embryos. (B) WISH for cmyb in 36 hpf dcn morphants (MOSTART) and their respective uninjected controls. Right panel indicates the numbers of cmyb+ cells in the dorsal aorta of control and dcn morphant embryos. (C) WISH for runx1 in 30 hpf dcn+/+ and dcn−/− embryos. Right panel indicates the numbers of runx1+ cells in the dorsal aorta of dcn+/+ and dcn−/− embryos. (D) WISH for cmyb in 36 hpf dcn+/+ and dcn−/− embryos. Right panel indicates the numbers of cmyb+ cells in the dorsal aorta of dcn+/+ and dcn−/− embryos. ****P<0.0001 using either a two-tailed unpaired t-test or a Mann–Whitney test (24-57 embryos were analyzed for each condition, from 1-3 independent experiments). Arrowheads indicate HSPCs. Data are mean±s.e.m. Scale bars: 300 µm.