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Polycomb-mediated axial patterning requires nucleosome compaction

ABSTRACT: Polycomb-mediated axial patterning requires nucleosome compaction

PROVIDER: PRJNA340227 | ENA |

REPOSITORIES: ENA

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Polycomb-mediated axial patterning requires nucleosome compaction [ChIP-seq]

Project description:We determined the genome-wide binding profiles of wild type and compaction mutant CBX2 (denoted as 'KRA') in mouse embryonic stem cells (mESCs) by ChIP-seq.

2017-08-31 | GSE86084 | GEO

Polycomb-mediated axial patterning requires nucleosome compaction

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-08-31 | GSE86085 | GEO

Polycomb-mediated axial patterning requires nucleosome compaction [RNA-seq]

Project description:We determined by RNA-seq gene expression changes in mESCs following the induced expression of WT-, KRA- or DEA-CBX2 variants in Cbx2 null cells.

2017-08-31 | GSE86083 | GEO

Mutation of a nucleosome compaction region disrupts Polycomb-mediated axial patterning.

Project description:Nucleosomes play important structural and regulatory roles by tightly wrapping the DNA that constitutes the metazoan genome. The Polycomb group (PcG) proteins modulate nucleosomes to maintain repression of key developmental genes, including Hox genes whose temporal and spatial expression is tightly regulated to guide patterning of the anterior-posterior body axis. CBX2, a component of the mammalian Polycomb repressive complex 1 (PRC1), contains a compaction region that has the biochemically defined activity of bridging adjacent nucleosomes. Here, we demonstrate that a functional compaction region is necessary for proper body patterning, because mutating this region leads to homeotic transformations similar to those observed with PcG loss-of-function mutations. We propose that CBX2-driven nucleosome compaction is a key mechanism by which PcG proteins maintain gene silencing during mouse development.

| S-EPMC5503153 | biostudies-literature

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.

2020-12-22 | GSE146301 | GEO

Mus musculus

Project description:Polycomb-mediated axial patterning requires nucleosome compaction [RNA-seq]

| PRJNA340229 | ENA

Mus musculus

Project description:Polycomb-mediated axial patterning requires nucleosome compaction [ChIP-seq]

| PRJNA340228 | ENA

Planarian yorkie/YAP functions to integrate adult stem cell proliferation, organ homeostasis, and maintenance of axial patterning

Project description:During adult homeostasis and regeneration, the freshwater planarian must accomplish a constant balance between cell proliferation and cell death, while also maintaining proper tissue and organ size and patterning. Yet how these ordered processes are precisely modulated, remains relatively unknown. Here we show that planarians use the downstream effector of the Hippo signalling cascade, yorkie (yki; YAP in vertebrates) to control a diverse set of pleiotropic processes in organ homeostasis, stem cell regulation, regeneration, and axial patterning. We show that yki functions to maintain the homeostasis of the planarian excretory (protonephridial) system and to limit stem cell proliferation, while not affecting the differentiation process or cell death. Finally, we show that yki synergizes with WNT/β-catenin signalling to repress head determination by limiting the expression domains of posterior WNT genes and the WNT-inhibitor notum. Together, our data show that yki is a key factor in planarians that integrates stem cell proliferation control, organ homeostasis, and the spatial patterning of tissues.

2015-10-03 | GSE73700 | GEO

Identification of direct transcriptional targets of BMP signaling during zebrafish dorsal-ventral axial patterning

Project description:Identification of direct transcriptional targets of BMP signaling during zebrafish dorsal-ventral axial patterning

| PRJNA684560 | ENA

Polycomb-mediated chromatin compaction during cell differentiation

Project description:Polycomb-mediated chromatin compaction during cell differentiation

| PRJNA354285 | ENA