Neural crest cells migrate extensively in vertebrate embryos to populate diverse derivatives including ganglia of the peripheral nervous system.
Molecular Events Controlling Cessation of Trunk Neural Crest Migration and Onset of Differentiation.
Specimen part
View SamplesUsing EphB2 or the ISC marker Lgr5, we have FACS-purified and profiled intestinal stem cells (ISCs), crypt proliferative progenitors and late transient amplifying cells to define a gene expression program specific for normal ISCs.
The intestinal stem cell signature identifies colorectal cancer stem cells and predicts disease relapse.
Specimen part
View SamplesSerotonin in the mammary gland is known to regulate processes such as calcium homeostasis, tight junction permeability, and milk protein gene expression. The objective of this study was to discover novel genes, pathways and functions which serotonin modulates during lactation. The rate-limiting enzyme in the synthesis of non-neuronal serotonin is tryptophan-hydroxylase (TPH1). Therefore, we used TPH1 knock-out mice dams (serotonin deficient) and compared them to wild-type dams and also Tph1 deficient dams injected daily with 5-HTP. Mammary gland tissues were collected on day 10 of lactation and then analyzed by RNA sequencing. Overall design: Genome-wide gene expression profiles of 12 mouse mammary gland samples were evaluated using RNA sequencing; these 12 samples belong to wild-type dams (WT; n = 4), Tryptophan hydroxylase (Tph1) knock-out dams (KO; Tph1 deficient; n = 4), and Tph1 deficient dams injected daily with 5-HTP (RC; n = 4). Mammary tissues were collected on day 10 of lactation and then underwent RNA extraction, library generation, and subsequent sequencing.
Transcriptomic Analysis of the Mouse Mammary Gland Reveals New Insights for the Role of Serotonin in Lactation.
No sample metadata fields
View SamplesThe PR domain containing 1a, with ZNF domain factor, gene prdm1a plays an integral role in the development of a number of different cell types during vertebrate embryogenesis, including neural crest cells, Rohon-Beard (RB) sensory neurons and the cranial neural crest-derived craniofacial skeletal elements. To better understand how Prdm1a regulates the development of various cell types in zebrafish, we performed a microarray analysis comparing wild type and prdm1a mutant embryos and identified a number of genes with altered expression in the absence of prdm1a. Rescue analysis determined that two of these, sox10 and islet1, lie downstream of Prdm1a in the development of neural crest cells and Rohon-Beard neurons, respectively. In addition, we identified a number of other novel downstream targets of Prdm1a that may be important for the development of diverse tissues during zebrafish embryogenesis.
prdm1a Regulates sox10 and islet1 in the development of neural crest and Rohon-Beard sensory neurons.
Age, Specimen part
View SamplesIn higher eukaryotes, an important mechanism to tune translation in different tissues and conditions is mTORC1-dependent regulation of tRNAs transcription by RNA polymerase III (Pol III), as the relative amount of tRNAs tightly coordinates with the translational needs of the cell. mTORC1 contributes to regulate protein synthesis through its direct substrate MAF1, which functions as a negative regulator of Pol III transcription in response to stimuli such as serum starvation or rapamycin treatment. Here, we applied ChIP-seq to examine the Pol III occupancy profile in human fibroblasts and report evidence of a genome wide, MAF1-dependent coordinated response to favorable or stress growth conditions. Strikingly, while a set of genes is extremely responsive in terms of Pol III binding, other genes are mostly unperturbed, yet associated with transcriptionally engaged polymerases as revealed by nascent EU-labeled RNA-seq (neuRNA-seq). As shown by DamIP-seq, the responsiveness of a subset of genes is tightly connected to the rapid and transient interaction of MAF1 with DNA-bound Pol III. Overall design: We performed duplicate ChIP-seq experiments for the Rpc4 (POLR3D) subunit of RNA polymerase III in IMR90hTert cells grown in the presence of fetal bovine serum (FBS), serum starved (SS), serum starved and treated with insulin (SS+I), serum starved and treated with insulin and rapamycin (SS+R+I). Additional ChIP-seq profiles were generated in cells treated with MAF1 siRNAs and serum starved. MAF1 binding was addressed by DamIP-seq, using two replicates per clone of IMR90hTert cells expressing HA-tagged MAF1-DamK9A (2 different clones) or EGFP-DamK9A (2 different clones). To monitor dynamic transcription profiles we did neusRNA-seq in IMR90hTert cells EU-labeled or mock (DMSO)-labeled. For both DamIP-seq and neusRNA-seq, cells were either unperturbed or serum starved.
Human MAF1 targets and represses active RNA polymerase III genes by preventing recruitment rather than inducing long-term transcriptional arrest.
No sample metadata fields
View SamplesUsing Next-generation sequencing (NGS) to get the retinal transcriptome profiles (RNA-seq) for understanding gene regulations during retina development Overall design: Retinal mRNA profiles from embryo day 16.5 to postnatal day 28 wild type (WT) mice were generated by NGS sequencing
Deletion of the Thyroid Hormone-Activating Type 2 Deiodinase Rescues Cone Photoreceptor Degeneration but Not Deafness in Mice Lacking Type 3 Deiodinase.
Cell line, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
The transcription factor GATA6 enables self-renewal of colon adenoma stem cells by repressing BMP gene expression.
Specimen part, Cell line
View SamplesAberrant activation of WNT signaling and loss of BMP signals represent the two main alterations leading to the initiation of colorectal cancer (CRC). Here we screen for genes required for maintaining the tumor stem cell phenotype and identify the zinc-finger transcription factor GATA6 as key regulator of the WNT and BMP pathways in CRC. GATA6 directly drives the expression of LGR5 in adenoma stem cells while it restricts BMP signaling to differentiated tumor cells. Genetic deletion of Gata6 in mouse colon adenomas increases the levels of BMP factors, which signal to block self-renewal of tumor stem cells. In human tumors, GATA6 competes with beta-catenin/TCF4 for binding to a distal regulatory region of the BMP4 locus that has been previously linked to increased susceptibility to develop CRC. Hence, GATA6 creates a permissive environment for tumor stem cell expansion by controlling the major signaling pathways that influence CRC initiation.
The transcription factor GATA6 enables self-renewal of colon adenoma stem cells by repressing BMP gene expression.
Specimen part, Cell line
View SamplesAberrant activation of WNT signaling and loss of BMP signals represent the two main alterations leading to the initiation of colorectal cancer (CRC). Here we screen for genes required for maintaining the tumor stem cell phenotype and identify the zinc-finger transcription factor GATA6 as key regulator of the WNT and BMP pathways in CRC. GATA6 directly drives the expression of LGR5 in adenoma stem cells while it restricts BMP signaling to differentiated tumor cells. Genetic deletion of Gata6 in mouse colon adenomas increases the levels of BMP factors, which signal to block self-renewal of tumor stem cells. In human tumors, GATA6 competes with beta-catenin/TCF4 for binding to a distal regulatory region of the BMP4 locus that has been previously linked to increased susceptibility to develop CRC. Hence, GATA6 creates a permissive environment for tumor stem cell expansion by controlling the major signaling pathways that influence CRC initiation.
The transcription factor GATA6 enables self-renewal of colon adenoma stem cells by repressing BMP gene expression.
Specimen part, Cell line
View SamplesHsa-miR-500a-5p (miR500a) activity has been associated with breast cancer survival.
miR-500a-5p regulates oxidative stress response genes in breast cancer and predicts cancer survival.
Specimen part, Cell line
View Samples