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OTT1 (RBM15 ) was originally described as a 5′ translocation partner of theMAL (MKL1 ) gene in t(1 ,22 )(p13;q13) infant acute mega karyocytic leukemia.OTT1 has no established physiological function, but it shares homology with thespen /Mint /SHARP family of proteins defined by three amino-terminal RNA recognition motifs and a carboxyl-terminal SPOC (Spen paralog and ortholog carboxyl-terminal) domain believed to act as a transcriptional repressor. To define the role ofOTT1 in hematopoiesis and help elucidate the mechanism of t(1 ,22 ) acute megakaryocytic leukemia pathogenesis, a conditional allele ofOtt1 was generated in mice. Deletion ofOtt1 in adult mice caused a loss of peripheral B cells due to a block in pro/pre-B differentiation. There is myeloid and megakaryocytic expansion in spleen and bone marrow, an increase in the Lin− Sca-1+ c-Kit+ compartment that includes hematopoietic stem cells, and a shift in progenitor fate toward granulocyte differentiation. These data show a requirement forOtt1 in B lymphopoiesis, and inhibitory roles in the myeloid, megakaryocytic, and progenitor compartments. The ability ofOtt1 to affect hematopoietic cell fate and expansion in multiple lineages is a novel attribute for aspen family member and delineatesOtt1 from other known effectors of hematopoietic development. It is plausible that dysregulation ofOtt1 -dependent hematopoietic developmental pathways, in particular those affecting the megakaryocyte lineage, may contribute toOTT1-MAL -mediated leukemogenesis.

Ott1 ( Rbm15 ) has pleiotropic roles in hematopoietic development