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NLRP7 promotes trophoblast lineage differentiation, YY1 binding and alters CpG methylation

ABSTRACT: Genome wide DNA methylation profiling of hESC in the untransduced, scrambled control and with knockdown of NLRP7 in undifferentiated and BMP4 differentiated states using the Illumina HumanMethylation 450 BeadChip. Several genomic sites exhibit altered methylation upon knocking down NLRP7.

ORGANISM(S): Homo sapiens

PROVIDER: GSE45727 | GEO | 2013/11/04

SECONDARY ACCESSION(S): PRJNA196136

REPOSITORIES: GEO

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NLRP7 promotes trophoblast lineage differentiation, YY1 binding and alters CpG methylation

Project description:Genome wide DNA methylation profiling of hESC in the untransduced, scrambled control and with knockdown of NLRP7 in undifferentiated and BMP4 differentiated states using the Illumina HumanMethylation 450 BeadChip. Several genomic sites exhibit altered methylation upon knocking down NLRP7. Bisulphite converted DNA from 3 replicates of untransduced, scrambled control and NLRP7 knockdown in the undifferentiated and BMP differentiated groups were hybridised to the Illumina Human Methylation 450 Beadchip.

2013-11-04 | E-GEOD-45727 | biostudies-arrayexpress

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Project description:The Illumina HumanMethylation 450 BeadChip was used on 20 matched pairs of early and late secondary gliomas to assess the changes in DNA methylation during progression.

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A Patient specific iPSC-based model of Hydatidiform mole reveals abnormal BMP4 signaling caused by NLRP7 deficiency

Project description:Complete Hydatidiform Mole (HM) is a gestational trophoblastic disease resulting in hyper proliferation of trophoblast cells and absence of embryo development. Mutations in NLRP7 gene is a major cause of familial recurrent complete HM, where no embryonic tissue is present during the pregnancy. NLRP7 is a novel protein and its function is poorly understood. Lack of NLRP7 in the mouse genome and challenges in studying human embryogenesis as well as human trophoblast differentiation has prevented elucidation of the pathophysiology of this disease and the function of NLRP7 in HM. Here, we established an in vitro model of HM using NLRP7 deficient patient-derived human induced pluripotent stem cells (iPSCs). Whole transcriptome profiling during trophoblast differentiation revealed that NLRP7 deficiency results in precocious downregulation of pluripotency factors, activation of trophoblast genes and promotes maturation of differentiated extraembryonic cell types such as syncytiotrophoblasts. We further showed that these phenotypes are dependent on BMP4 signaling and BMP pathway inhibition prevented excessive trophoblast differentiation of HM-iPSCs. Taken together, this novel human iPSC model of a genetic placental disease recapitulates aspect of trophoblast biology and sheds light on early human embryogenesis by identifying NLRP7 as an important regulator of this process.

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Project description:The Illumina HumanMethylation 450 BeadChip was used on 20 matched pairs of early and late secondary gliomas to assess the changes in DNA methylation during progression. Bisulphite converted DNA from the 40 samples were hybridised to the Illumina Infinium 450k Human Methylation Beadchip.

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NLRP7 affects trophoblast lineage differentiation, binds to overexpressed YY1 and alters CpG methylation.

Project description:Maternal-effect mutations in NLRP7 cause rare biparentally inherited hydatidiform moles (BiHMs), abnormal pregnancies containing hypertrophic vesicular trophoblast but no embryo. BiHM trophoblasts display abnormal DNA methylation patterns affecting maternally methylated germline differentially methylated regions (gDMRs), suggesting that NLRP7 plays an important role in reprogramming imprinted gDMRs. How NLRP7-a component of the CATERPILLAR family of proteins involved in innate immunity and apoptosis-causes these specific DNA methylation and trophoblast defects is unknown. Because rodents lack NLRP7, we used human embryonic stem cells to study its function and demonstrate that NLRP7 interacts with YY1, an important chromatin-binding factor. Reduced NLRP7 levels alter DNA methylation and accelerate trophoblast lineage differentiation. NLRP7 thus appears to function in chromatin reprogramming and DNA methylation in the germline or early embryonic development, functions not previously associated with members of the NLRP family.

| S-EPMC3888260 | biostudies-literature

DNA methylation data from 12 normal and 10 chronic periodontitis patients from site OCI

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Project description:Genomic instability is the main cause of abnormal embryo development and abortion. NLRP7 dysfunctions affect embryonic development and lead to recurrent pregnancy loss (RPL) or hydatidiform moles (HM), but the underlying mechanisms remain largely elusive. In this study, we found that NLRP7 knockout affected the genetic stability, resulting in increased DNA damage in both human embryonic stem cells (hESCs) and blastoids, making embryonic cells in blastoids more susceptible to apoptosis. Mechanistically, NLRP7 could interact with factors related to alternative splicing (AS) and DNA damage response (DDR), including DDX39B, PRPF8, THRAP3 and PARP1, and its dysfunction led to abnormal AS of genes involved in Homologous recombination (HR) in hESCs, indicating that NLRP7-mediated AS is required for the maintenance of genome integrity during early human embryogenesis. Together, this study first uncovers that NLRP7 plays an essential role in the maintenance of genetic stability during early human embryonic development by regulating AS of HR-related genes.

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Array-based profiling of the lymphoma cell DNA methylome does not unequivocally distinguish primary lymphomas of the central nervous system from non-CNS diffuse large B-cell lymphomas

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