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Trim28 Haploinsufficiency Triggers Bi-stable Epigenetic Obesity

ABSTRACT: Trim28 Haploinsufficiency Triggers Bi-stable Epigenetic Obesity

PROVIDER: PRJEB11740 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR1227660_1.fastq.gz	Fastqsanger.gz
	ERR1227660_2.fastq.gz	Fastqsanger.gz
	ERR1227670_1.fastq.gz	Fastqsanger.gz
	ERR1227670_2.fastq.gz	Fastqsanger.gz
	ERR1227680.fastq.gz	Fastqsanger.gz

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Trim28 Haploinsufficiency Triggers Bi-stable Epigenetic Obesity.

Project description:More than one-half billion people are obese, and despite progress in genetic research, much of the heritability of obesity remains enigmatic. Here, we identify a Trim28-dependent network capable of triggering obesity in a non-Mendelian, "on/off" manner. Trim28(+/D9) mutant mice exhibit a bi-modal body-weight distribution, with isogenic animals randomly emerging as either normal or obese and few intermediates. We find that the obese-"on" state is characterized by reduced expression of an imprinted gene network including Nnat, Peg3, Cdkn1c, and Plagl1 and that independent targeting of these alleles recapitulates the stochastic bi-stable disease phenotype. Adipose tissue transcriptome analyses in children indicate that humans too cluster into distinct sub-populations, stratifying according to Trim28 expression, transcriptome organization, and obesity-associated imprinted gene dysregulation. These data provide evidence of discrete polyphenism in mouse and man and thus carry important implications for complex trait genetics, evolution, and medicine.

| S-EPMC4735019 | biostudies-literature

MOF haploinsufficiency triggers diet-induced obesity resistance

Project description:MOF haploinsufficiency triggers diet-induced obesity resistance

| PRJNA658027 | ENA

MOF haploinsufficiency triggers diet-induced obesity resistance (RNA-seq)

Project description:MOF haploinsufficiency triggers diet-induced obesity resistance (RNA-seq)

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MOF haploinsufficiency triggers diet-induced obesity resistance (ChIP-seq)

Project description:MOF haploinsufficiency triggers diet-induced obesity resistance (ChIP-seq)

| PRJNA658033 | ENA

TAB2 haploinsufficiency

Project description:TAB2 haploinsufficiency

| PRJNA747894 | ENA

TRIM28 is essential for erythroblast differentiation in the mouse

Project description:We discovered that Trim28 genetic loss in the adult mouse leads to defective immature erythropoiesis in the bone marrow and consequently to anemia.We further found that TRIM28 controls erythropoiesis in a cell-autonomous manner by inducibly deleting Trim28 exclusively in hematopoietic cells. Finally, in the absence of TRIM28 we observed increased apoptosis as well as diminished expression of multiple erythroid transcription factors and heme biosynthetic enzymes in immature erythroid cells. Thus, TRIM28 is essential for the cell-autonomous development of immature erythroblasts in the bone marrow. To induce Cre recombinase from the Mx1Cre transgene, poly(I:C) was injected 5 times every other day. Mice were analyzed two weeks after completion of poly(I:C) administration. TRIM28 mutant mice generate two distinct types of immature erythroid cells; KOa, with 5-8% of the Trim28 gene remaining undeleted (still bearing 26% of residual mRNA), and KOb, with 1-4% of the gene remaining undeleted (and with 18% of mRNA remaining).

2013-10-04 | E-GEOD-49843 | biostudies-arrayexpress

RNA-seq of gonadal adipose tissue from male and female Trim28-WT and Trim28 adipose specific KO mice

Project description:Many genes have been implicated in WAT lipid metabolism, including tripartite motif containing 28 (Trim28), a gene proposed to primarily influence adiposity via epigenetic mechanisms in embryonic development. We set out to determine if adipose specific deletion of Trim28 led to changes in adipose tissue function and molecular phenotype. We performed transcriptomics analysis on adipose tissue taken from WT and adipose specific Trim28 KO mice to investigate their molecular phenotype, and to identify pathways altered in KO animals.

2020-11-25 | E-MTAB-9809 | biostudies-arrayexpress

TRIM28 silences endogenous retroviruses in neural progenitor cells

Project description:Here we show that in neural progenitor cells (NPCs) TRIM28 silences transcription of two groups of endogenous retroviruses (ERVs): IAP1 and MMERVK10C. Derepression of ERVs in Trim28-deficient NPCs was associated with a loss of H3K9me3 and resulted in transcriptional upregulation and reverse transcription. These findings demonstrate a unique dynamic transcriptional regulation of ERVs in NPCs. Analysis of upregulation of ERVs in Trim28-deficient NPCs

2015-01-07 | E-GEOD-45930 | biostudies-arrayexpress

Twist1-Haploinsufficiency Selectively Enhances the Osteoskeletal Capacity of Mesoderm-derived Parietal Bone through Downregulation of Fgf23

Project description:Purpose: This study investigates the postnatal impact of Twist1 haploinsufficiency on the osteoskeletal ability and regeneration on two calvarial bones arising from tissues of different embryonic origin: the neural crest-derived frontal and the mesoderm-derived parietal bones. Results: Twist1 haplonsufficiency selectively enhanced osteogenic and tissue regeneration ability of mesoderm-derived parietal bones. Twist1 haplonsufficiency triggers its selective activity on mesoderm-derived parietal bone through downregulation of the bone-derived hormone Fgf23. Conclusions: Twist1 haploinsufficiency preferentially triggers osteogenic induction of parietal bones which may be beneficial to optimize treatments for skeletal regeneration, reconstruction and repair of mesoderm-derived bone, as well as to alleviate skeletal abnormalities caused by Twist1 haploinsufficiency.

2018-09-15 | GSE119962 | GEO

TRIM28 regulates RNA polymerase II promoter proximal pausing and entry into processive elongation

Project description:Analysis of total PolII and Ser2-phosphorylated PolII genomic occupancy in control-transfected (WT) or Trim28-knockdown (Trim28-KD) embryonic stem cells. Embryonic stem cells were transfected with luciferase siRNA (WT) or Trim28 siRNA (Trim28 KD) in duplicate experiments. 48 hrs after transfection, cells were crosslinked with formaldehyde, collected, lysed, and chromatin was fragmented with sonication. Total PolII or Ser2-phosphorylated PolII genomic occupancy in WT or Trim28 KD cells were determined by ChIP-seq.

2014-07-28 | E-GEOD-48253 | biostudies-arrayexpress

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