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LaminB1 DamID in HT1080 fibroblasts overexpressing NET29/TMEM120A, NET39/PPAPDC3 or NET47/TM7SF2

ABSTRACT: Maps of genomic regions in proximity to the nuclear lamina were determined in untreated HT1080 fibroblasts and HT1080 stable cell lines expressing NET29/TMEM120A, NET39/PPAPDC3 or NET47/TM7SF2 as GFP fusions

ORGANISM(S): Homo sapiens

PROVIDER: GSE87148 | GEO | 2016/12/31

SECONDARY ACCESSION(S): PRJNA343797

REPOSITORIES: GEO

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Transcriptome analysis of human HT1080 cells overexpressing full length or soluble nucleoplasmic fragment of NET29/TMEM120A, NET39/PPAPDC3 and NET47/TM7SF2

Project description:The nuclear transmembrane proteins (NETs) NET29/TMEM120A, NET39/PPAPDC3 and NET47/TM7SF2 are able to reposition chromosomes towards/away from the nuclear envelope when overexpressed or knocked down in HT1080 cells. In this study we wanted to investigate the transcriptome changes after transfection of the full length NETs or a nucleoplasmic soluble fragment that does not localise to the nuclear envelope.

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LaminB1-DamID analysis of differentiating 3T3L1 mouse pre-adipocytes with knock-down of Tmem120a and Tmem120b

Project description:Maps of genomic regions in proximity to the nuclear lamina were determined in undifferentiated 3T3L1 preadipocytes and 9 day differentiated (wild type, and under Tmem120a or Tmem120a/b knockdown) adipocytes using DamID with a Dam-Lamin B1-encoding lentivirus.

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Project description:LaminB1 DamID in HT1080 fibroblasts overexpressing NET29/TMEM120A, NET39/PPAPDC3 or NET47/TM7SF2

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RNA-seq analysis of subcutaneus inguinal adipose tissue from Tmem120a fat specific knockout mice (females)

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The nuclear envelope protein Net39 is essential for muscle nuclear integrity and chromatin organization

Project description:Lamins and transmembrane proteins within the nuclear envelope regulate nuclear structure and chromatin organization. Nuclear Envelope Transmembrane Protein 39 (Net39) is muscle nuclear envelope protein whose functions in vivo have not been explored. We show that mice lacking Net39 succumb to severe myopathy and juvenile lethality, with concomitant disruption in nuclear integrity, chromatin accessibility, gene expression and metabolism. These abnormalities resemble those of Emery-Dreifuss muscular dystrophy (EDMD), caused by mutations in A-type Lamins (LMNA) and other genes, like Emerin (EMD). We observe that Net39 is downregulated in EDMD patients, implicating Net39 in the pathogenesis of this disorder. Our findings highlight the role of Net39 at the nuclear envelope in maintaining muscle chromatin organization, gene expression and function, and its potential contribution to the molecular etiology of EDMD.

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Net39 protects muscle nuclei from mechanical stress during the pathogenesis of Emery-Dreifuss muscular dystrophy [snRNA-seq]

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