PhD student in Pathology and Cell Biology
Université de Montréal
Award-winning publication: SMARCD2 subunit of SWI/SNF chromatin-remodeling complexes mediates granulopoiesis through a CEBPɛ dependent mechanism
Published in: Nature Genetics
SWI/SNF chromatin remodeling complexes have been studied for several years for the critical role they play in cell growth and differentiation. Recent sequencing has pointed the finger at the mutation of a number of subunits of the SWI/SNF complex in nearly 20% of cancers and other human pathologies, including myelodysplastic syndrome (the accumulation of immature, non-functional blood cells). Relying on a mouse model modified using a genetic deletion technique that suppresses the SMARCD2 gene, Pierre Priam and his team demonstrated that the Baf60b protein encoded by the SMARCD2 gene is key to the collaboration between the SWI/SNF complex and a transcription factor (a protein that controls the expression of a gene set) known as CEBPɛ, which is vital to the development of neutrophilic granulocytes. The study results confirm that when the collaboration is interrupted, CEBPɛ can no longer regulate its target genes, causing the granulocytes to stop differentiating and thus collect in the bone marrow in an immature, non-functional state. These findings contribute to the advancement of knowledge in hematopoiesis and epigenetics.