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High Density Domain-Focused CRISPR Screens Reveal Novel Epigenetic Regulators of HOX/MEIS Activation in Acute Myeloid Leukemia [RNA-seq, SGF29 KO vs. NTC in MOLM13 and U937]

ABSTRACT: High Density Domain-Focused CRISPR Screens Reveal Novel Epigenetic Regulators of HOX/MEIS Activation in Acute Myeloid Leukemia [RNA-seq, SGF29 KO vs. NTC in MOLM13 and U937]

PROVIDER: PRJNA1020747 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26160504_1.fastq.gz	Fastqsanger.gz
	SRR26160504_2.fastq.gz	Fastqsanger.gz
	SRR26160505_1.fastq.gz	Fastqsanger.gz
	SRR26160505_2.fastq.gz	Fastqsanger.gz
	SRR26160506_1.fastq.gz	Fastqsanger.gz

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High Density Domain-Focused CRISPR Screens Reveal Novel Epigenetic Regulators of HOX/MEIS Activation in Acute Myeloid Leukemia [RNA-seq, SGF29 KO vs. NTC in MOLM13 and U937]

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The Epigenetic Regulator Landscape of HOX/MEIS Expression in AML [scRNA-seq]

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Axial skeleton anterior-posterior patterning is regulated through feedback regulation between Meis and retinoic acid

Project description:Vertebrate axial skeletal patterning is controlled by coordinated collinear expression of Hox genes and axial level-dependent activity of Hox protein combinations. Transcription factors of the Meis family act as cofactors of Hox proteins and profusely bind to Hox complex DNA, however their roles in mammalian axial patterning have not been established. Similarly, retinoic acid (RA) is known to regulate axial skeletal element identity through the transcriptional activity of its receptors, however whether this role is related to Meis/Hox regulation or functions in axial patterning remains unknown. Here we study the role of Meis factors in axial skeleton formation and its relationship to the RA pathway by characterizing Meis1, Meis2 and Raldh2 mutant mice. We report that Meis and Raldh2 regulate each other in a positive feedback regulatory loop that controls axial skeletal identity. Meis elimination produces homeotic transformations similar to those found in Raldh2 and anterior-Hox mutants and disrupts the expression of Hox target genes without changing the transcriptional profiles of Hox complexes. We propose that Meis regulates vertebrate axial skeleton patterning by exclusively affecting Hox protein function, and that alterations in RA levels can produce homeotic transformations without altering Hox transcription through regulating Meis expression.

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Project description:Meis1 and Meis2 are highly similar homeodomain transcription factors that regulate organogenesis through cooperation with Hox proteins. Overexpression experiments have suggested an essential role for Meis factors in limb proximo-distal patterning; however, loss-of-function experiments supporting this notion have not been reported. Meis1 and Meis2 are coexpressed during limb development, first in the lateral plate mesoderm, before limb induction, and then they become restricted to a proximal domain of the growing limb bud. Here, we report that complete double conditional Meis1/2 inactivation in the lateral plate mesoderm leads to limb agenesis. Meis factors cooperate with Tbx factors in this function, extensively co-binding with Tbx to genomic sites and co-regulating enhancers of fgf10, a critical factor in limb initiation. Limbs with three deleted Meis alleles develop a complete PD set of limb skeletal elements, but show proximal-specific skeletal hypoplasia and agenesis of posterior skeletal elements. This failure in posterior skeletal element specification reveals an early role of Meis factors in establishing the limb AP prepattern required for Shh activation at later stages. Our results uncover novel roles for Meis transcription factors in early limb development and identify their involvement in new molecular interaction networks that regulate organogenesis.

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Meis IBA ChIP-seq

Project description:Chromatin immunoprecipitation using pan-Meis antibodies in first branchial arch cells from E11.5 mouse embryos detected by SOLiD sequencing

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MEIS homeodomain proteins facilitate PARP1/ARTD1-mediated eviction of histone H1

Project description:Pre–B-cell leukemia homeobox (PBX) and myeloid ecotropic viral integration site (MEIS) proteins control cell fate decisions in many physiological and pathophysiological contexts, but how these proteins function mechanistically remains poorly defined. Focusing on the first hours of neuronal differentiation of adult subventricular zone–derived stem/progenitor cells, we describe a sequence of events by which PBX-MEIS facilitates chromatin accessibility of transcriptionally inactive genes: In undifferentiated cells, PBX1 is bound to the H1-compacted promoter/proximal enhancer of the neuron-specific gene doublecortin (Dcx). Once differentiation is induced, MEIS associates with chromatin-bound PBX1, recruits PARP1/ARTD1, and initiates PARP1-mediated eviction of H1 from the chromatin fiber. These results for the first time link MEIS proteins to PARP-regulated chromatin dynamics and provide a mechanistic basis to explain the profound cellular changes elicited by these proteins.

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