Chromosome dosage plays a significant role in reproductive isolation and speciation in both plants and animals, but underlying mechanisms are largely obscure. Transposable elements can promote hybridity through maternal small RNA, and have been postulated to regulate dosage response via neighboring imprinted genes. Here, we show that a highly conserved microRNA in plants, miR845, targets the tRNAMet primer-binding site (PBS) of LTR-retrotransposons in Arabidopsis pollen, and triggers the accumulation of 21 to 22-nucleotide small RNA in a dose dependent fashion via RNA polymerase IV. We show that these epigenetically activated small-interfering RNAs (easiRNAs) mediate hybridization barriers between diploid seed parents and tetraploid pollen parents (“the triploid block”), and that natural variation for miR845 may account for “endosperm balance” allowing formation of triploid seeds. Targeting the PBS with small RNA is a common mechanism for transposon control in mammals and plants, and provides a uniquely sensitive means to monitor chromosome dosage and imprinting in the developing seed. Overall design: RNA-seq of Arabidopsis pollen
Transposon-derived small RNAs triggered by miR845 mediate genome dosage response in Arabidopsis.
Specimen part, Subject
View SamplesHere we used microarray expression profiling to characterise global changes in gene expression during stages of proliferation and differentiation of human neural stem cells
Associations of the Intellectual Disability Gene MYT1L with Helix-Loop-Helix Gene Expression, Hippocampus Volume and Hippocampus Activation During Memory Retrieval.
Specimen part, Cell line
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DIDO as a Switchboard that Regulates Self-Renewal and Differentiation in Embryonic Stem Cells.
Specimen part
View SamplesTransition from symmetric to asymmetric cell division requires precise coordination of differential gene expression. Embryonic stem cells (ESC) strongly express Dido3, whose C-terminal truncation impedes ESC differentiation while retaining self-renewal. We show that Dido3 binds to its gene locus via H3K4me3 and RNA pol II and, at differentiation onset, induces expression of its splice variant Dido1, which then leads to Dido3 degradation and downregulation of stemness genes. We propose that Dido isoforms act as a switchboard to regulate genetic programs for ESC transition from pluripotency maintenance to promotion of differentiation.
DIDO as a Switchboard that Regulates Self-Renewal and Differentiation in Embryonic Stem Cells.
Specimen part
View SamplesWe conditionally knocked out both Yap and Taz in cranial neural crest (CNC) using the Wnt1Cre driver and sequenced mRNA from embryonic day 10.5 mandibles. Overall design: Examination of mRNA level in E10.5 mandibular tissues from control and Wnt1Cre Taz and Yap dKO mutant.
Yap and Taz play a crucial role in neural crest-derived craniofacial development.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Mutant human embryonic stem cells reveal neurite and synapse formation defects in type 1 myotonic dystrophy.
No sample metadata fields
View SamplesAnalysis of genes that were differentially expressed in mutant VUB03_DM1 as compared to controls VUB01 and SA01 Neural Precursor cells
Mutant human embryonic stem cells reveal neurite and synapse formation defects in type 1 myotonic dystrophy.
No sample metadata fields
View SamplesAnalysis of genes that were differentially expressed in mutant VUB03_DM1 as compared to controls VUB01 and SA01 undifferentiated hES cells
Mutant human embryonic stem cells reveal neurite and synapse formation defects in type 1 myotonic dystrophy.
No sample metadata fields
View SamplesAnalysis of genes that were differentially expressed in mutant VUB03_DM1 as compared to controls VUB01 and SA01 Mesodermal Precursors Cells.
Mutant human embryonic stem cells reveal neurite and synapse formation defects in type 1 myotonic dystrophy.
No sample metadata fields
View SamplesThis experiment was carried out in the context of a pharmacogenetic study of long-term (4-year follow-up) response to Interferon-beta treatment in two cohorts of Italian Multiple Sclerosis patients, to identify genetic variants (SNPs) that may influence response to IFN-beta. We integrated results from meta-analysis of the two cohorts with gene expression profiling of IFN stimulated PBMCs from 20 healthy controls and eQTL analyses, to look at possible enrichment of IFN-beta induced genes with genes mapped by top-ranking meta-analyzed SNPs.
Pharmacogenetic study of long-term response to interferon-β treatment in multiple sclerosis.
Sex, Specimen part, Disease, Disease stage, Subject
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