The aim of this data set is to perform a differential expression analysis between wild type eye-antennal imaginal disc and discs that are homozygous glass mutant gl[60j]. This data set is used to validate Glass target gene predictions identified by i-cisTarget on a set of conserved eye-specific genes. Overall design: RNA-seq was performed in eye-antennal imaginal discs of two D.melanogaster wild-type strains (Canton S and strain RAL-208 (Jordan et al. 2007, Ayroles et al. 2009)), representing two biological replicates; and in glass mutant (gl[60j]) discs for two technical replicates.
Comparative motif discovery combined with comparative transcriptomics yields accurate targetome and enhancer predictions.
Specimen part, Cell line, Subject
View SamplesThe aim of this project was to evaluate the ploidy of a S. cerevisiae *S. kudriavzevii hybrid in comparison to the lab strain S288C. Other wine yeast have been icluded in the project for the global analysis.
Ecological success of a group of Saccharomyces cerevisiae/Saccharomyces kudriavzevii hybrids in the northern european wine-making environment.
No sample metadata fields
View SamplesMicrophthalmos is a rare congenital anomaly characterized by reduced eye size and visual deficits of variable degrees. Sporadic and hereditary microphthalmos has been associated to heterozygous mutations in genes fundamental for eye development. Yet, many cases are idiopathic or await the identification of molecular causes. Here we show that haploinsufficiency of Meis1, a transcription factor with an evolutionary conserved expression in the embryonic trunk, brain and sensory organs, including the eye, causes microphthalmic traits and visual impairment, in adult mice. In the trunk, Meis1 acts as a cofactor for genes of the Hox complex, mostly binding to Hox-Pbx target sequence on the DNA. By combining the analysis of Meis1 loss-of-function and conditional Meis1 functional rescue with ChIPseq and RNAseq approaches, we show that during the development of the optic cup, an Hox-free region, Meis1 binds instead to Hox/Pbx-independent Meis binding site, and coordinates, in a dose-dependent manner, retinal proliferation and differentiation by regulating the expression of components of the Notch signalling pathway. Meis1 also controls the activity of genes responsible for human microphthalmia and eye patterning so that in Meis1-/- embryos, the eye size is reduced and boundaries among the different eye territories are shifted or blurred. We thus propose that Meis1 is at the core of a genetic network implicated in microphthalmia, itself representing an additional candidate for syndromic cases of these ocular malformations. Overall design: Transcriptomics and Meis1 Occupancy analysis on mouse isolated optic cups and ChIP data for histone methylation marks were obtained from about 100 eyes of E10.5 CD1 embryos.
Meis1 coordinates a network of genes implicated in eye development and microphthalmia.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Discovery of first-in-class reversible dual small molecule inhibitors against G9a and DNMTs in hematological malignancies.
Cell line, Treatment
View SamplesThe indisputable role of epigenetics in cancer and the fact that epigenetic alterations can be reversed have favored development of epigenetic drugs. In this study, we have design and synthesize potent novel, selective and reversible chemical probes that simultaneously inhibit the G9a and DNMTs methyltransferase activity. In vitro treatment of hematological neoplasia (Acute Myeloid Leukemia-AML, Acute Lymphoblastic Leukemia-ALL and Diffuse Large B-cell Lymphoma-DLBCL) with the lead compound CM-272, inhibited cell proliferation and promoted apoptosis, inducing interferon stimulated genes and immunogenic cell death. CM-272 significantly prolonged survival of AML, ALL and DLBCL xenogeneic models. Our results represent the discovery of first-in-class dual inhibitors of G9a/DNMTs and establish this chemical series, as a promising therapeutic tool for unmet needs in hematological tumors.
Discovery of first-in-class reversible dual small molecule inhibitors against G9a and DNMTs in hematological malignancies.
Cell line, Treatment
View SamplesMinichromosome maintenance (MCM) proteins facilitate replication by licensing origins and unwinding the DNA double strand. Interestingly, the number of MCM hexamers greatly exceeds the number of firing origins suggesting additional roles of MCMs. Here we show a hitherto unanticipated function of MCM2 in cilia formation in human cells and zebrafish that is uncoupled from replication. Zebrafish depleted of MCM2 develop ciliopathy-phenotypes including microcephaly and aberrant heart looping due to malformed cilia. In non-cycling human fibroblasts, loss of MCM2 promotes transcription of a subset of genes, which cause cilia shortening and centriole overduplication. Chromatin immunoprecipitation experiments show that MCM2 binds to transcription start sites of cilia inhibiting genes. We propose that such binding may block RNA polymerase II-mediated transcription. Depletion of a second MCM (MCM7), which functions in complex with MCM2 during its canonical functions, reveals an overlapping cilia-deficiency phenotype likely unconnected to replication, although MCM7 appears to regulate a distinct subset of genes and pathways. Our data suggests that MCM2 and 7 exert a role in ciliogenesis in post-mitotic tissues. Overall design: 6 samples in total: 3 control, 3 siRNA MCM7
Resting cells rely on the DNA helicase component MCM2 to build cilia.
Specimen part, Cell line, Treatment, Subject
View SamplesMinichromosome maintenance (MCM) proteins facilitate replication by licensing origins and unwinding the DNA double strand. Interestingly, the number of MCM hexamers greatly exceeds the number of firing origins suggesting additional roles of MCMs. Here we show a hitherto unanticipated function of MCM2 in cilia formation in human cells and zebrafish that is uncoupled from replication. Zebrafish depleted of MCM2 develop ciliopathy-phenotypes including microcephaly and aberrant heart looping due to malformed cilia. In non-cycling human fibroblasts, loss of MCM2 promotes transcription of a subset of genes, which cause cilia shortening and centriole overduplication. Chromatin immunoprecipitation experiments show that MCM2 binds to transcription start sites of cilia inhibiting genes. We propose that such binding may block RNA polymerase II-mediated transcription. Depletion of a second MCM (MCM7), which functions in complex with MCM2 during its canonical functions, reveals an overlapping cilia-deficiency phenotype likely unconnected to replication, although MCM7 appears to regulate a distinct subset of genes and pathways. Our data suggests that MCM2 and 7 exert a role in ciliogenesis in post-mitotic tissues. Overall design: 6 samples in total: 3 control, 3 siRNA MCM2
Resting cells rely on the DNA helicase component MCM2 to build cilia.
Specimen part, Cell line, Treatment, Subject
View SamplesUV-B radiation affects leaf growth in a wide range of species. In this work, we demonstrate that UV-B levels present in solar radiation inhibits maize leaf growth without causing any other visible stress symptoms, including accumulation of DNA damage. We conducted kinematic analyses of cell division and expansion to understand the impact of UV-B radiation on these cellular processes. Our results demonstrate that the decrease in leaf growth is a consequence of a reduction in cell production, and a shortened growth zone (GZ) in UV-B irradiated leaves. To determine the molecular pathways involved in UV-B inhibition of leaf growth, we performed RNA sequencing on isolated GZ tissues of control and UV-B exposed plants. Our results show a link between the observed leaf growth inhibition and the expression of specific cell cycle and developmental genes, including Growth Regulating Factors (GRFs) and transcripts for proteins participating in different hormone pathways. Overall design: Factorial design with two factors: Treatment (control vs UV-B) x Zone I (0-1cm from base of the leaf), 2 (1-2cm from base of the leaf) and 3 (2-3cm from base of the leaf), 3 replicates
UV-B Inhibits Leaf Growth through Changes in Growth Regulating Factors and Gibberellin Levels.
Specimen part, Subject
View SamplesP1 encodes an R2R3-MYB transcription factor responsible for the accumulation of insecticidal flavones in maize silks and red phlobaphene pigments in pericarps and other floral tissues, which contributed to making P1 an important visual marker since the dawn of modern genetics. We conducted RNA-Seq using pericarps at two different stages, 14 and 25 days after pollination (DAP). High-throughput sequencing using the Illumina platform resulted in the generation of ~20 million high quality reads, from which ~90% aligned to the recently completed maize genome sequence corresponding to ~5 million reads for each one of the four samples. Overall design: Examination of two different RNA samples from two different stages of maize pericarp tissues.
A genome-wide regulatory framework identifies maize pericarp color1 controlled genes.
Specimen part, Subject
View SamplesP1 encodes an R2R3-MYB transcription factor responsible for the accumulation of insecticidal flavones in maize silks and red phlobaphene pigments in pericarps and other floral tissues, which contributed to making P1 an important visual marker since the dawn of modern genetics. We conducted RNA-Seq using from maize silks obtained at 2-3 days after emergence. High-throughput sequencing using the Illumina platform resulted in the generation of ~14 million high quality reads, corresponding to ~7 million reads for each sample, from which 76% aligned to the maize genome. Overall design: Examination of two different RNA samples from maize silks obtained at 2-3 days after emergence
A genome-wide regulatory framework identifies maize pericarp color1 controlled genes.
Specimen part, Subject
View Samples