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Several signaling pathways control blood cell (hemocyte) development in the  Drosophila  lymph gland. Mechanisms that modulate and integrate these signals are poorly understood. Here we report that mutation in a conserved endocytic protein Asrij affects signal transmission and causes aberrant lymph gland hematopoiesis. Mammalian Asrij (Ociad1) is expressed in stem cells of the blood vascular system and is implicated in several cancers. We found that  Drosophila  Asrij is a pan-hemocyte marker and localizes to a subset of endocytic vesicles. Loss of  asrij  causes hyperproliferation of lymph gland lobes coupled with increased hemocyte differentiation, thereby depleting the pool of quiescent hemocyte precursors. This co-relates with fewer Col+ cells in the hematopoietic stem cell niche of  asrij  mutants.  Asrij  null mutants also show excess specification of crystal cells that express the RUNX factor Lozenge (Lz), a target of Notch signaling.  Asrij  mutant lymph glands show increased N in sorting endosomes suggesting aberrant trafficking.  In vitro  assays also show impaired traffic of fluorescent probes in  asrij  null hemocytes. Taken together our data suggest a role for Asrij in causing increased Notch signaling thereby affecting hemocyte differentiation. Thus, conserved endocytic functions may control blood cell progenitor quiescence and differentiation.

Asrij Maintains the Stem Cell Niche and Controls Differentiation during Drosophila Lymph Gland Hematopoiesis