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XB-IMG-84641

Xenbase Image ID: 84641


Figure 6. Tel1-Dependent VEGFA in the DLP and in the Somites Drives HSC Development (A) Schematic depiction of experimental design. Wild-type or MO-injected two cell embryos were cultured to stage 22 when DLPs and/or somites were explanted and cultured separately or together until sibling embryos had reached stage 27/28. RNA was extracted from the test DLPs and assayed for Scl expression normalized to ODC. Error bars indicate the SEM. (B) Induction of Scl expression in the DLP is tissue autonomous. DLPs at stage 22 (sample 1), expressing no Scl, express substantial quantities when cultured to stage 27/28 (sample 2). (C) Loss of Scl expression in the DLP of Tel1 morphants (sample 3) can be rescued by coculture with wild-type somitic tissue (sample 5), but not with wild-type DLP tissue (sample 4) or somitic tissue injected with either VegfA MO (sample 6) or Tel1 MO (sample 7). (D) Tissue-autonomous expression of Scl is dependent on VEGFA. The robust expression in wild-type DLPs (sample 2) is abolished by VegfA MO injection (sample 8). (E) Model illustrating the contribution of Tel1 and VEGFA to HSC development. Correct programming of adult hemangioblasts, the earliest precursors of HSCs, requires VEGFA signaling. Endogenous (adult hemangioblast) and exogenous (somites) VEGFA, controlled by Tel1, is required. Although hemangioblasts are not correctly programmed in the absence of Tel1, DA precursors are capable of migrating to the midline, where VEGFA is still produced in the hypochord (see Figure 4B). VEGFA signaling in the midline also appears to be sufficient for the endothelial differentiation and lumenization of a vessel in the position of the DA. Critically, though, the DA is not specified as an artery, hematopoiesis fails, and HSCs are not produced. Genes downregulated and cell types not specified in Tel1 morphants are indicated in red. See also Figure S1 and Table S2.

Image published in: Ciau-Uitz A et al. (2010)

Copyright © 2010. Image reproduced on Xenbase with permission of the Publisher, Elsevier B. V.

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