Scott W. Boyer
University of California, Santa Cruz
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Publication
Featured researches published by Scott W. Boyer.
Experimental Hematology | 2014
Anna E. Beaudin; Scott W. Boyer; E. Camilla Forsberg
Defining differentiation pathways is central to understanding the pathogenesis of hematopoietic disorders, including leukemia. The function of the receptor tyrosine kinase Flk2 (Flt3) in promoting myeloid development remains poorly defined, despite being commonly mutated in acute myeloid leukemia. We investigated the effect of Flk2 deficiency on myelopoiesis, focusing on specification of progenitors between HSC and mature cells. We provide evidence that Flk2 is critical for proliferative expansion of multipotent progenitors that are common precursors for all lymphoid and myeloid lineages, including megakaryocyte/erythroid (MegE) cells. Flk2 deficiency impaired the generation of both lymphoid and myeloid progenitors by abrogating propagation of their common upstream precursor. At steady state, downstream compensatory mechanisms masked the effect of Flk2 deficiency on mature myeloid output, whereas transplantation of purified progenitors revealed impaired generation of all mature lineages. Flk2 deficiency did not affect lineage choice, thus dissociating the role of Flk2 in promoting cell expansion and regulating cell fate. Surprisingly, despite impairing myeloid development, Flk2 deficiency afforded protection against myeloablative insult. This survival advantage was attributed to reduced cell cycling and proliferation of progenitors in Flk2-deficient mice. Our data support the existence of a common Flk2(+) intermediate for all hematopoietic lineages and provide insight into how activating Flk2 mutations promote hematopoietic malignancy by non-Flk2-expressing myeloid cells.
Cell Cycle | 2012
Scott W. Boyer; Anna E. Beaudin; E. Camilla Forsberg
Genetic fate-mapping approaches provide a unique opportunity to assess differentiation pathways under physiological conditions. We have recently employed a lineage tracing approach to define hematopoietic differentiation pathways in relation to expression of the tyrosine kinase receptor Flk2.1 Based on our examination of reporter activity across all stem, progenitor and mature populations in our Flk2-Cre lineage model, we concluded that all mature blood lineages are derived through a Flk2+ intermediate, both at steady-state and under stress conditions. Here, we re-examine in depth our initial conclusions and perform additional experiments to test alternative options of lineage specification. Our data unequivocally support the conclusion that onset of Flk2 expression results in loss of self-renewal but preservation of multilineage differentiation potential. We discuss the implications of these data for defining stem cell identity and lineage potential among hematopoietic populations.
Immunity | 2013
Daigo Hashimoto; Andrew Chow; Clara Noizat; Pearline Teo; Mary Beth Beasley; Marylene Leboeuf; Christian Becker; Peter See; Jeremy Price; Daniel Lucas; Melanie Greter; Arthur Mortha; Scott W. Boyer; E. Camilla Forsberg; Masato Tanaka; Nico van Rooijen; Adolfo García-Sastre; E. Richard Stanley; Florent Ginhoux; Paul S. Frenette; Miriam Merad
Cell Stem Cell | 2011
Scott W. Boyer; Aaron V. Schroeder; Stephanie Smith-Berdan; E. Camilla Forsberg
Cell Stem Cell | 2016
Anna E. Beaudin; Scott W. Boyer; Jessica Perez-Cunningham; Gloria Hernandez; S. Christopher Derderian; Chethan Jujjavarapu; Eric Aaserude; Tippi C. MacKenzie; E. Camilla Forsberg
Experimental Hematology | 2018
Smrithi Rajendiran; Scott W. Boyer; Anna E. Beaudin; Jana Krietsch; Camilla Forsberg
Experimental Hematology | 2014
Anna E. Beaudin; S. Chris Derderian; Scott W. Boyer; Tippi C. MacKenzie; Camilla Forsberg
Blood | 2014
Anna E. Beaudin; Scott W. Boyer; Gloria Hernandez; Camilla Forsberg
Experimental Hematology | 2013
Anna E. Beaudin; Scott W. Boyer; E. Camilla Forsberg