ChIP-seq of ASXL2 in SKNO1 cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE84363 | GEO | 2017/06/26
SECONDARY ACCESSION(S): PRJNA329034
REPOSITORIES: GEO
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Project description:The goals of this study are to identify the changes of H3K27Ac in SKNO1 cells after knockdown of ASXL2
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Project description:The goals of this study are to compare transcriptome profiling (RNA-seq) of Asxl2 knockdowned SKNO-1 cells to control SKNO-1 cells. We found substantial number of genes are differentially expressed in Asxl2 knockdowned cells.
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Project description:An imbalance in the activities of the Polycomb and Trithorax complexes underlies numerous human pathologies, including cancer. The BAP1 deubiquitinase (DUB) complex negatively regulates Polycomb activity and also recruits the Trithorax histone H3K4 methyltransferase, MLL3/COMPASS, to the enhancers of tumor suppressor genes. We and others have demonstrated that the BAP1-MLL3 pathway is mutated in several differ cancers. Yet, how BAP1 recruits MLL3 to these loci remains a fundamentally important unanswered question. Here we demonstrate that ASXL2 directly mediates the interaction between the BAP1 complex and MLL3/COMPASS. ASXL2 loss abolishes the MLL3-BAP1 interaction, leading to decreased MLL3 occupancy at enhancers and reduced expression of BAP1-MLL3 target genes. The interaction between ASXL2 and MLL3 is negatively regulated by protein arginine methyltransferase 4 (PRMT4, also known as CARM1), which methylates ASXL2 on R639/R641. Methylation of ASXL2 by CARM1 blocks binding to MLL3 binding and impairs the expression of MLL3 dependent genes. This finding uncovers a novel transcription repression function for CARM1 and provides a unique insight into the BAP1/ASXL2/MLL3 axis, which is controlled by arginine methylation and could serve as a target for potential cancer therapeutics.
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Project description:Chromosomal translocation t(8;21) (q22;q22) leading to generation of oncogenic RUNX1-RUNX1T1 (AML1-ETO) fusion is a cytogenetic abnormality observed in about 10% of acute myelogenous leukemia (AML). To uncover somatic mutations that cooperate with t(8;21)-driven leukemia, we performed targeted and whole exome sequencing of newly-diagnosed and relapsed AML samples. We identified high frequency of truncating alterations in ASXL2 along with recurrent mutations of KIT, TET2, MGA, FLT3, and DHX15 in this subtype of AML. To investigate in-depth the role of ASXL2 in normal and malignant hematopoiesis, we utilized a mouse model of ASXL2 deficiency. Loss of ASXL2 caused progressive hematopoietic defects characterized by myeloid cell expansion, splenomegaly, extramedullary hematopoiesis and poor reconstitution ability in transplantation models. A parallel analysis of young and >1-year old Asxl2-deficient mice revealed age-dependent changes in the hematopoietic compartment leading to perturbations affecting not only myeloid and erythroid differentiation but also maturation of lymphoid cells. Our studies also suggest that expression of truncated ASXL2 protein confers proliferative advantage to mouse myeloid progenitors. Overall, these findings establish a critical role of ASXL2 in maintaining steady state hematopoiesis and provide insights into how its loss/mutation primes leukemic growth of myeloid cells.
2018-12-01 | GSE106796 | GEO
Project description:Chromosomal translocation t(8;21) (q22;q22) leading to generation of oncogenic RUNX1-RUNX1T1 (AML1-ETO) fusion is a cytogenetic abnormality observed in about 10% of acute myelogenous leukemia (AML). To uncover somatic mutations that cooperate with t(8;21)-driven leukemia, we performed targeted and whole exome sequencing of newly-diagnosed and relapsed AML samples. We identified high frequency of truncating alterations in ASXL2 along with recurrent mutations of KIT, TET2, MGA, FLT3, and DHX15 in this subtype of AML. To investigate in-depth the role of ASXL2 in normal and malignant hematopoiesis, we utilized a mouse model of ASXL2 deficiency. Loss of ASXL2 caused progressive hematopoietic defects characterized by myeloid cell expansion, splenomegaly, extramedullary hematopoiesis and poor reconstitution ability in transplantation models. A parallel analysis of young and >1-year old Asxl2-deficient mice revealed age-dependent changes in the hematopoietic compartment leading to perturbations affecting not only myeloid and erythroid differentiation but also maturation of lymphoid cells. Our studies also suggest that expression of truncated ASXL2 protein confers proliferative advantage to mouse myeloid progenitors. Overall, these findings establish a critical role of ASXL2 in maintaining steady state hematopoiesis and provide insights into how its loss/mutation primes leukemic growth of myeloid cells.
2018-12-01 | GSE106797 | GEO