SWI/SNF Complex Prevents Lineage Reversion and Induces Temporal Patterning in Neural Stem Cells | Zendy

Elif Eroğlu | Zendy; Thomas R. Burkard | Zendy; Yanrui Jiang | Zendy; Nidhi Saini | Zendy; Catarina C. F. Homem | Zendy; Heinrich Reichert | Zendy; Juergen A. Knoblich | Zendy

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SWI/SNF Complex Prevents Lineage Reversion and Induces Temporal Patterning in Neural Stem Cells

Author(s) -

Elif Eroğlu,

Thomas R. Burkard,

Yanrui Jiang,

Nidhi Saini,

Catarina C. F. Homem,

Heinrich Reichert,

Juergen A. Knoblich

Publication year - 2014

Publication title -

cell

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 26.304

H-Index - 776

eISSN - 1097-4172

pISSN - 0092-8674

DOI - 10.1016/j.cell.2014.01.053

Subject(s) - biology , carcinogenesis , neural stem cell , swi/snf , stem cell , neuroblast , genetics , lineage (genetic) , progenitor cell , chromatin , microbiology and biotechnology , cancer stem cell , chromatin remodeling , gene , neurogenesis

Members of the SWI/SNF chromatin-remodeling complex are among the most frequently mutated genes in human cancer, but how they suppress tumorigenesis is currently unclear. Here, we use Drosophila neuroblasts to demonstrate that the SWI/SNF component Osa (ARID1) prevents tumorigenesis by ensuring correct lineage progression in stem cell lineages. We show that Osa induces a transcriptional program in the transit-amplifying population that initiates temporal patterning, limits self-renewal, and prevents dedifferentiation. We identify the Prdm protein Hamlet as a key component of this program. Hamlet is directly induced by Osa and regulates the progression of progenitors through distinct transcriptional states to limit the number of transit-amplifying divisions. Our data provide a mechanistic explanation for the widespread tumor suppressor activity of SWI/SNF. Because the Hamlet homologs Evi1 and Prdm16 are frequently mutated in cancer, this mechanism could well be conserved in human stem cell lineages. PAPERCLIP:

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