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Abstract
Primitive erythropoiesis, the formation of the embryo’s first red blood cells, is controlled by GATA‑dependent signals within blood‑fated cells and their surrounding environment. Using Xenopus laevis, this dissertation identifies two distinct regulatory roles for GATA factors. First, we show that the GATA co‑factor FOG is essential for primitive erythropoiesis; FOG depletion causes apoptosis of primitive erythrocytes, and structure‑function studies reveal a critical requirement for FOG interaction with the NuRD complex. Second, we demonstrate that ectodermal GATA‑2 regulates primitive erythropoiesis through reciprocal control of canonical and non‑canonical Wnt signaling and through activation of a novel GATA‑2 target, xTRIL. These findings highlight cell‑autonomous and non‑autonomous mechanisms by which GATA factors orchestrate early blood development.