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

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

PROVIDER: PRJNA751990 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15338269_1.fastq.gz	Fastqsanger.gz
	SRR15338269_2.fastq.gz	Fastqsanger.gz
	SRR15338270_1.fastq.gz	Fastqsanger.gz
	SRR15338270_2.fastq.gz	Fastqsanger.gz
	SRR15338271_1.fastq.gz	Fastqsanger.gz

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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

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 [cHi-C]

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

| PRJNA751985 | 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 [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: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 [ChIP-seq]

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

2021-10-05 | GSE181383 | 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

Breakpoints around the HOXD cluster result in various limb malformations.

Project description:BackgroundCharacterisation of disease associated balanced chromosome rearrangements is a promising starting point in the search for candidate genes and regulatory elements.MethodsWe have identified and investigated three patients with limb abnormalities and breakpoints involving chromosome 2q31. Patient 1 with severe brachydactyly and syndactyly, mental retardation, hypoplasia of the cerebellum, scoliosis, and ectopic anus, carries a balanced t(2;10)(q31.1;q26.3) translocation. Patient 2, with translocation t(2;10)(q31.1;q23.33), has aplasia of the ulna, shortening of the radius, finger anomalies, and scoliosis. Patient 3 carries a pericentric inversion of chromosome 2, inv(2)(p15q31). Her phenotype is characterised by bilateral aplasia of the fibula and the radius, bilateral hypoplasia of the ulna, unossified carpal bones, and hypoplasia and dislocation of both tibiae.ResultsBy fluorescence in situ hybridisation, we have mapped the breakpoints to intervals of approximately 170 kb or less. None of the three 2q31 breakpoints, which all mapped close to the HOXD cluster, disrupted any known genes.ConclusionsHoxd gene expression in the mouse is regulated by cis-acting DNA elements acting over distances of several hundred kilobases. Moreover, Hoxd genes play an established role in bone development. It is therefore very likely that the three rearrangements disturb normal HOXD gene regulation by position effects.

| S-EPMC2564623 | biostudies-literature

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