Reduction of T antigen causes loss of hematopoietic progenitors in Drosophila through the inhibition of filopodial extensions from the hematopoietic niche

•Plasmatocyte-secreted T antigens maintain hematopoietic stem cells in Drosophila.•Filopodial extension from hematopoietic niche is disrupted in dC1β3GalT1 mutants.•Tn antigen-positive materials cover lymph gland primary lobe in dC1β3GalT1 larvae.•Ectopically deposited hemolectin disrupts stem cell maintenance.•Filopodial extension is inhibited by a hemolectin-containing clotting shell.

Hematopoietic stem cells (HSCs) are present in hematopoietic organs and differentiate into mature blood cells as required. Defective HSCs have been implicated in the human autoimmune disease Tn syndrome, which results from the failure of the core 1 β1,3-galactosyltransferase 1 enzyme (C1β3GalT1) to synthesize T antigen. In both mice and humans, a reduced level of T antigen is associated with a reduction in blood cell numbers. However, the precise roles of T antigen in hematopoiesis are unknown. Here, we show that the Drosophila T antigen, supplied by plasmatocytes, is essential for the regulation of HSCs. T antigen appears to be an essential factor in maintaining the extracellular environment to support filopodial extensions from niches that are responsible for transmitting signaling molecules to maintain the HSCs. In addition, our results revealed that the clotting factor, hemolectin, disrupted the hemolymph environment of C1β3GalT1 mutants. This study identified a novel mucin function for the regulation of HSCs that may be conserved in other species.

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