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Cumulative in-cis mutagenesis in vivo reveals various functions for CTCF sites at the mouse Hoxd cluster [cHi-C]

ABSTRACT: Cumulative in-cis mutagenesis in vivo reveals various functions for CTCF sites at the mouse Hoxd cluster [cHi-C]

PROVIDER: PRJNA751985 | ENA |

REPOSITORIES: ENA

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Cumulative in-cis mutagenesis in vivo reveals various functions for CTCF sites at the mouse Hoxd cluster [cHi-C]

Project description:We used Capture Hi-C enriching the Hoxd locus and its flanking TADs to study the effects of CRISPR/Cas9-induced CTCF binding sites deletions on chromatin architecture. We analysed wildtype and homozygous mutant E9.5 trunks and E12.5 distal and proximal forelimbs.

2021-10-05 | GSE181386 | GEO

Cumulative in-cis mutagenesis in vivo reveals various functions for CTCF sites at the mouse Hoxd cluster

Project description:Cumulative in-cis mutagenesis in vivo reveals various functions for CTCF sites at the mouse Hoxd cluster

| PRJNA751874 | ENA

Cumulative in-cis mutagenesis in vivo reveals various functions for CTCF sites at the mouse Hoxd cluster [ChIPmentation]

Project description:Cumulative in-cis mutagenesis in vivo reveals various functions for CTCF sites at the mouse Hoxd cluster [ChIPmentation]

| PRJNA751990 | ENA

Cumulative in-cis mutagenesis in vivo reveals various functions for CTCF sites at the mouse Hoxd cluster [RNA-seq]

Project description:Cumulative in-cis mutagenesis in vivo reveals various functions for CTCF sites at the mouse Hoxd cluster [RNA-seq]

| PRJNA751984 | ENA

Cumulative in-cis mutagenesis in vivo reveals various functions for CTCF sites at the mouse Hoxd cluster [ChIP-seq]

Project description:Cumulative in-cis mutagenesis in vivo reveals various functions for CTCF sites at the mouse Hoxd cluster [ChIP-seq]

| PRJNA751992 | ENA

Cumulative in-cis mutagenesis in vivo reveals various functions for CTCF sites at the mouse Hoxd cluster

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

2021-10-05 | GSE181387 | GEO

Cumulative in-cis mutagenesis in vivo reveals various functions for CTCF sites at the mouse Hoxd cluster [ChIPmentation]

Project description:ChIPmentation-seq analysis of CTCF and RAD21 in wildtype and mutant CTCF binding sites alleles

2021-10-05 | GSE181384 | GEO

Cumulative in-cis mutagenesis in vivo reveals various functions for CTCF sites at the mouse Hoxd cluster [RNA-seq]

Project description:RNA-seq analysis of the effect of CRISPR/Cas9-induced CTCF binding sites deletions on gene expression. We studied E12.5 distal or proximal forelimbs of wildtype and mutant alleles.

2021-10-05 | GSE181385 | GEO

Cumulative in-cis mutagenesis in vivo reveals various functions for CTCF sites at the mouse Hoxd cluster [ChIP-seq]

Project description:ChIP-seq analysis of CTCF wildtype in mouse embryonic posterior trunk and brain samples

2021-10-05 | GSE181383 | GEO

Mesomelic Dysplasias Associated With The HOXD Locus Are Caused By Regulatory Reallocations [cHi-C]

Project description:Some human families display severe shortening and bending of the radius and ulna, a condition referred to as mesomelic dysplasia. Many of these families contain chromosomal rearrangements at 2q31, where the human HOXD locus maps. In mice, the dominant X-ray-induced Ulnaless inversion of the HoxD gene cluster produces a similar phenotype suggesting that the same pathological mechanism is at work in humans and mice. A tentative hypothesis was proposed where the various alterations to the genomic structure of HOXD could translocate Hoxd13 near to proximal limb enhancers, leading to its deleterious gain-of-expression in the embryonic forelimb. We evaluated this hypothesis by engineering a ca. 1Mb large inversion including the HoxD gene cluster, in order to position Hoxd13 within a chromatin domain rich in proximal limb enhancers. We show that these enhancers contact and activate Hoxd13 in proximal cells, concomitant to the formation of a mesomelic dysplasia phenotype. A secondary mutation in the coding frame of the HOXD13 protein in-cis with the inversion completely rescued the limb alterations, demonstrating that ectopic HOXD13 is indeed the unique cause of this bone anomaly. Single cell expression analysis and evaluation of HOXD13 binding sites in cells from this ectopic expression domain suggests that the phenotype arises primarily by acting through genes normally controlled by HOXD13 in distal limb cells. Altogether, these results provide a conceptual and mechanistic framework to understand and unify the molecular origins of human mesomelic dysplasia associated with 2q31.

2021-07-20 | GSE165491 | GEO

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