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Genome-wide DNA methylation analysis of diploid hydatidiform moles with androgenetic or biparental genomic origin

ABSTRACT: Only very few studies have investigated methylation patterns of different types of hydatidiform moles (HMs). Methylation patterns of androgenetic HMs (AnHMs) are abnormal due to the fact that the nuclear genome in AnHMs is inherited from the father, only. Diploid biparental HMs (BiHM) have been suggested to display the same methylation patterns of imprinted genes as AnHMs, and the methylation patterns are suspected to be a consequence of a failure to establish maternal methylation at multiple genome-wide loci. We have investigated the methylation patterns of AnHMs, BiHM-like placentas with a chr. 11p15.5 deletion and a BiHM from a woman with NLRP7 mutations and compared these to methylation patterns of normal placentas. Using the Next Generation Sequencing (NGS) technique Reduced Representation Bisulfite Sequencing (RRBS) we instigated the genome-wide CpG methylation of 32 samples, including nine normal placentas, 20 androgenetic diploid HMs (AnHMs), and three diploid biparental HMs/HM-like placentas. This dataset contains RRBS data from 12 samples, including the nine normal placentas and the three diploid biparental HMs/HM-like placentas.The RRBS data from 20 androgenetic diploid HMs (AnHMs) was deposited in GSE65881:http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE65881

ORGANISM(S): Homo sapiens

PROVIDER: GSE67412 | GEO | 2015/06/01

SECONDARY ACCESSION(S): PRJNA279851

REPOSITORIES: GEO

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Project description:Heterochromatin plays a key role in gene repression, maintaining genome integrity and chromosome segregation. Fission yeast, Schizosaccharomyces pombe, utilizes conserved components to direct heterochromatin formation using siRNA generated by RNA interference (RNAi) to guide a histone H3 lysine 9 methyltransferase to cognate chromatin. To identify compounds that inhibit heterochromatin formation, an in vivo phenotypic screen for loss of silencing was performed. A tester strain harbouring a silent dominant selectable kanMX reporter gene within fission yeast centromeric heterochromatin was used to screen a diverse library of chemicals. HMS-I1 and HMS-I2 were identified as compounds that reproducibly increased G418 resistance due to loss of kanMX silencing, and decreased the level of repressive H3K9 methylation on centromeric repeats. The pattern of changes induced by HMS-I1 and HMS-I2 were consistent with inhibition of the histone deacetylases (HDACs) Clr3 and/or Sir2. Chemical-genetic interactions and expression profiling indicated that both HMS-I1 and HMS-I2 affect the activity of the Clr3-containing Snf2/HDAC repressor complex (SHREC). Exposure to HMS-I1 was also found to alleviate silencing of reporter genes in an Arabidopsis transgenic plant line and a mouse cell line. HMS-I2 also disrupted reporter gene silencing in Arabidopsis. In vitro assays indicate that HMS-I1 impairs the activity of human HDAC6 and HDAC10. As HMS-I1 and HMS-I2 bear no resemblance to known inhibitors of chromatin-based activities they represent potentially novel and valuable reagents for experimental and therapeutic purposes. Our findings highlight the use of in vivo chemical screening conducted in fission yeast to identify compounds that disrupt heterochromatin across plant, fungi and animal kingdoms. 16 RNA samples: 2 replicates of WT untreated (vehicle DMSO) (KE1-A, KE2-A), HMS-I1 treated (KE1-B, KE2-B), HMS-I2 treated (KE1-C, KE2-C), and 2 additional replicates of WT (KE05_wt_1, KE10_wt_2), 4 replicates of clr2M-bM-^HM-^F (KE01_2118_1, KE06_2118_2, KE03_0080_1, KE08_0080_2) and mit1M-bM-^HM-^F (KE02_1295_1, KE07_1295_2, KE04_1278_1, KE09_1278_2).

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Genome-wide DNA methylation analysis of diploid hydatidiform moles with androgenetic or biparental genomic origin

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