RNA-seq of diploid and triploid parthenogenetic human embryonic stem cells
Ontology highlight
ABSTRACT:
INSTRUMENT(S): NextSeq 500
ORGANISM(S): Homo sapiens
SUBMITTER: Guy Haim Abadi
PROVIDER: E-MTAB-11430 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:The systematic deep sequencing analysis provided a comprehensive understanding of the transcriptome complexity of 2n and 3n Fujian oyster. This information broadens our understanding of the mechanisms of C.angulata polyploidization and contributes to molecular and genetic research by enriching the oyster database. This is the first report on genome-wide transcriptional analysis of adductor muscle of diploid and triploid Fujian oyster and has demonstrated triploid oysters are morphologically almost identical to their diploid counterparts, but have faster growth, due to the reorientation of energetic allocation from gametogenesis to somatic investment. This study provides a foundation for further analysis of the gene expression patterns and signaling pathways which regulate the molecular mechanisms of diploid and triploid oyster. Examination of 3 different samples, including diploid (DF and DM) and triplod(T) oyster.
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Project description:To examain effects of triploidy on gene expression in mouse cells, we have employed whole genome microarray expression profiling. To study the effects of aneuploidy in mouse cells, we isorated diploid, triploid and tetraploid cells from p53-/- mouse embryonic cells Gene expression in diploid cells (RRI2, 15 and 2-1), triploid cells (RRI2-5, 2-12 and 2-15) and tetraploid cells (RRI2-2, 2-4 and 2-6).
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Project description:Dosage compensation restores a balanced network of gene expression between autosomes and sex chromosomes in males (XY) and females (XX). In mammals, this is achieved by doubling the expression of X-linked genes in both sexes, together with X inactivation in females. X up-regulation may be controlled by DNA sequence based and/or epigenetic mechanisms that double the X output potentially in response to an autosomal counting factor. Human triploids with either one or two active X chromosomes (Xa) provide a mean to test X chromosome expression in the presence of three sets of autosomes, which will help understand the underlying mechanisms of X up-regulation. We measured whole genome gene expression in human triploid cell cultures with either one or two active X. We found that overall X-linked gene expression is not tripled in the presence of three sets of autosomes. However, in triploid cells with a single active X chromosome, its expression is adjusted upward, presumably by an epigenetic mechanism that senses the active X-autosome ratio.
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