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Dev Biol. 2015 May 15;401(2):206-19. doi: 10.1016/j.ydbio.2015.03.003. Epub 2015 Mar 14.

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

Author information

1
Laboratory of Cell Biology, Department of Bioinformatics, Faculty of Engineering, Soka University, 1-236 Tangi-cho, Hachioji, Tokyo 192-8577, Japan.
2
Laboratory of Cell Biology, Department of Bioinformatics, Faculty of Engineering, Soka University, 1-236 Tangi-cho, Hachioji, Tokyo 192-8577, Japan. Electronic address: shoko@soka.ac.jp.

Abstract

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.

KEYWORDS:

Core 1 β1,3-galactosyltransferase 1; Drosophila; Filopodial extension; Hematopoietic stem cell; Hemolectin; T antigen

PMID:
25779703
DOI:
10.1016/j.ydbio.2015.03.003
[Indexed for MEDLINE]
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