Pleomorphic adenoma gene 1 (PLAG1) encodes a transcription factor involved in cancer and growth. We study the role of PLAG1 in preimplantation embryos using STRT RNA-seq of single embryos from wild type and knockout mothers (both mated with wild type studs). The lack of maternal Plag1 led to delayed mouse 2-cell stage embryo development, compensatory expression of Plag1 from the paternal allele, and dysregulation of 1,089 genes. Half of these genes displayed a pattern of delayed activation and play roles in ribosome biogenesis and protein synthesis. These mouse genes further showed a significant overlap with human EGA genes with similar ontology, and an enrichment of the PLAG1 de novo motif. We conclude that Plag1 affects EGA through retrotransposons influencing ribosomes and protein synthesis, a mechanism that might also explain its roles in cancer and growth Overall design: Single wild type and maternal Plag1 knockout embryos at MII, 2-cell and 8-cell stage development in 14-16 biologicla replicas per developmental stage and genotype.
Pleomorphic Adenoma Gene 1 Is Needed For Timely Zygotic Genome Activation and Early Embryo Development.
Subject
View SamplesCircuit neuroscience has made great progress by linking neuronal function to marker gene expression, allowing the specific investigation of otherwise indistinguishable neuronal ensembles. Here, we performed next generation sequencing on two functionally and genetically distinct interneuronal populations marked by the expression of protein kinase C d (PKCd) or somatostatin (SST) in the central amygdala (CEA) of mice, which are known to play distinct and sometimes opposing roles in emotion processing. Making their gene expression profile known will aid in forming hypotheses of how different neurotransmitters or psychoactive drugs could alter information processing in these neurons. Overall design: Unchallenged gene expression profile of two different neuronal populations in the central amygdala
Dorsal tegmental dopamine neurons gate associative learning of fear.
Sex, Specimen part, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Altering TET dioxygenase levels within physiological range affects DNA methylation dynamics of HEK293 cells.
Specimen part, Cell line, Treatment
View SamplesWe compared TET1 and TET3 overexpressing cells to uninduced cells with endogenous levels of the respective transcript to determine global gene expression changes.
Altering TET dioxygenase levels within physiological range affects DNA methylation dynamics of HEK293 cells.
Specimen part, Treatment
View SamplesWe used microarrays to study the changes in the transcriptional profile upon Snail knockdown in murine lung adenocarcinomas
Snail mediates repression of the Dlk1-Dio3 locus in lung tumor-infiltrating immune cells.
Age, Specimen part
View SamplesWe used microarrays to study the changes in the transcriptional profile upon Snail overexpression in murine lung adenocarcinomas
Snail mediates repression of the Dlk1-Dio3 locus in lung tumor-infiltrating immune cells.
Age, Specimen part
View SamplesWe compared TET triple knockdown cells to control cells treated with non-targeting siRNAs to determine global gene expression changes.
Altering TET dioxygenase levels within physiological range affects DNA methylation dynamics of HEK293 cells.
Cell line, Treatment
View SamplesBackground: NK cells during chronic viral infection have been well studied over the last decade. We performed an unbiased next-generation RNA-sequencing approach to identify commonalities or differences of the effect of HIV, HCV and HBV viremia on NK cell transcriptomes. Methods: Using cell sorting, we obtained CD3-CD56+ NK cells from blood of 6 HIV, 11 HCV, and 32 HBV infected and untreated patients. Library preparation and sequencing were done using Illumina mRNA-Seq Sample Prep Kit and the HiSeq 2000, HiSeq2500 or NextSeq 500, and further analysis by an in-house analytic pipeline. Results: In NK cells from HIV, HCV and HBV patients, transcriptome analysis identified 272, 53, and 56 differentially expressed genes, respectively (fold change >1.5, q-value 0.2). Interferon stimulated genes were induced in NK cells from HIV/HCV patients, but not during HBV infection. HIV viremia downregulated ribosome assembly genes in NK cells. In HBV, viral load and ALT variation had little effect on genes related to NK effector function. Conclusion: We compare, for the first time, NK cell transcripts of viremic HIV, HCV and HBV patients. We clearly demonstrate distinctive NK cell gene signatures in 3 different populations, suggestive for a different degree of functional alterations of the NK cell compartment as compared to healthy individuals. Overall design: We analyzed NK cell transcripts collected from the blood of well-characterized chronic HBV patients (n=32), chronic HCV patients (n=8), and HIV patients (n=6). Differential gene expression analysis, global module analysis, and unsupervised clustering analysis were performed by employing RNA-sequencing on blood NK cell transcriptomes.
Persistent Replication of HIV, Hepatitis C Virus (HCV), and HBV Results in Distinct Gene Expression Profiles by Human NK Cells.
Sex, Specimen part, Disease, Subject
View SamplesPrimary pre-B acute lymphoblastic (ALL) cells do not proliferate long-term ex vivo without the presence of stromal support. We developed and use an ex vivo co-culture model, consisting of mouse leukemic pre-B Bcr/Abl-expressing ALL cells grown with mitotically inactivated mouse embryonic fibroblasts (MEFs). This system provides a generic type of environmentally-mediated protection to the ALL cells, because when the ALL cells are treated with a moderate dose of a therapeutic drug, drug-resistant ALL cells can be recovered after a 1-2 week period of culture. Some of the factors produced by stromal cells that provide protection to ALL cells have been identified. However, it is unclear if the presence of drug-treated ALL cells affects the stromal fibroblasts. The current study was initiated to examine this using expression profiling on the irradiated MEFs.
Expression of cassini, a murine gamma-satellite sequence conserved in evolution, is regulated in normal and malignant hematopoietic cells.
Specimen part
View SamplesEML1 and EML3 were previously shown to be histone readers involved in plant-pathogen interactions. To learn more about the developmental function of EML1 and EML3, we generated eml1 eml3 double mutant and showed that it had specific seed developmental phenotypes, including a capability to develop seed without fertilization. Next, we analyzed the mRNA expression of genes in the eml1 eml3 double mutant and compared it to its wild type. Differentially expressed (DE) genes in the mutant were identified and compared with DE of the mutants known to be involved in regulating seed development and in fertilization-independent endosperm development. Our results suggest that some targets are shared between EML histone readers and known regulators of seed development, such as MEA. Auxin response seems to be affected in both types of mutants. However, unlike MEA, EML proteins regulate auxin responsive genes not only in the endosperm, but also in the embryo. This capability makes EML proteins very good candidates for engineering apomictic seeds. Overall design: 3 eml1,eml3 double mutant samples and 3 WT samples
Arabidopsis EMSY-like (EML) histone readers are necessary for post-fertilization seed development, but prevent fertilization-independent seed formation.
Specimen part, Subject
View Samples