This SuperSeries is composed of the SubSeries listed below.
Polo-Like Kinase 3 Appears Dispensable for Normal Retinal Development Despite Robust Embryonic Expression.
Specimen part
View SamplesThese data investigate the transcriptomic differences in the whole retinas of mice resulting from loss of Polo-like Kinase 3 (Plk3) over various stages of development, including adulthood, postnatal day (P)7, and P0.
Polo-Like Kinase 3 Appears Dispensable for Normal Retinal Development Despite Robust Embryonic Expression.
Specimen part
View SamplesAnalysis of adult retinas from tripartite motif-containing domain 9 knockouts and wild type littermates. Trim9 belongs to the TRIM family of E3 ubiquitin ligases. Results provide insight into possible roles for Trim9 in the retina.
The Trim family of genes and the retina: Expression and functional characterization.
Specimen part
View SamplesThese data investigate the transcriptomic differences in the whole retinas of mice resulting from loss of Polo-like Kinase 3 (Plk3) at embryonic day (E)16.
Polo-Like Kinase 3 Appears Dispensable for Normal Retinal Development Despite Robust Embryonic Expression.
Specimen part
View SamplesThis study aimed to characterize the transcriptomes of developing neurons from the chicken retina.
Single cell transcriptome profiling of developing chick retinal cells.
Specimen part, Time
View SamplesThis study aimed to characterize the transcriptomes of adult retinal ganglion cells (RGCs). The physiological properties of these cells were characterized first in non-dissociated retinal tissue. With that information recorded, the cells were isolated for transcriptome profiling.
Molecular signatures of retinal ganglion cells revealed through single cell profiling.
Specimen part
View SamplesMalformations of cortical development are the underlying eitiology of many cases of Mental Retardation and Epilepsy. Subtle, below the resolution of current MRI, cortical dysplasias are probably involved in many cases of MR, Epilepsy and Autism for which no diagnosis can currently be made. Therefore, understanding the process of cortical development will be vital in diagnosing and eventual treatment of many patients with these conditions. More specifically, the cortex forms from two major populations of neuroblasts which reach their final destination in the cortex by differerent mechanisms. One is radial migration from ventricular neuroblasts to the cortical plate. These cells are excititory projection neurons and glia. The second pathway is from the ventral ganglionic eminences and tangential migration of the interneuronal population of primarily inhibitory neurons. Much less is known about the control of the latter process, and many of these currently undiagnosed subtle malformations may stem from abnormalities of this tangential migration. This project focuses on the understanding the control of the tangentially migrating inhibitory interneurons.
Identification of Arx transcriptional targets in the developing basal forebrain.
No sample metadata fields
View SamplesArx is a paired-box homeodomain transcription factor and the vertebrate ortholog to the Drosophila aristaless (al) gene. Mutations in Arx are associated with a variety of human diseases, including X-linked infantile spasm syndrome (OMIM: 308350), X-linked myoclonic epilepsy with mental retardation and spasticity (OMIM: 300432), X-linked lissencephaly with ambiguous genitalia (OMIM: 300215), X-linked mental retardation 54 (OMIM: 300419), and agenesis of the corpus callosum with abnormal genitalia (OMIM: 300004). Arx-deficient mice exhibit a complex, pleiotrophic phenotype, including decreased proliferation of neuroepithelial cells of the cortex, dysgenesis of the thalamus and olfactory bulbs, and abnormal nonradial migration of GABAergic interneurons. It has been suggested that deficits in interneuron specification, migration, or function lead to loss of inhibitory neurotransmission, which then fails to control excitatory activity and leads to epilepsy or spasticities. Given that Arx mutations are associated with developmental disorders in which epilepsy and spasticity predominate and that Arx-deficient mice exhibit deficits in interneuron migration, understanding the function of Arx in interneuron migration will prove crucial to understanding the pathology underlying interneuronopathies. Yet, downstream transcriptional targets of Arx, to date, remain unidentified.
Identification of Arx transcriptional targets in the developing basal forebrain.
No sample metadata fields
View SamplesPancreatic islet endocrine cell and endothelial cell (EC) interactions mediated by vascular endothelial growth factor-A (VEGF-A) signaling are important for islet endocrine cell differentiation and the formation of highly vascularized islets. To dissect how VEGF-A signaling modulates intra-islet vasculature and innervation, islet microenvironment, and ß cell mass, we transiently increased VEGF-A production by ß cells. VEGF-A induction dramatically increased the number of intra-islet ECs but led to ß cell loss. After withdrawal of the VEGF-A stimulus, ß cell mass, function, and islet structure normalized as a result of a robust, but transient, burst in proliferation of pre-existing ß cells. Bone marrow-derived macrophages (MFs) recruited to the site of ß cell injury were crucial for the ß cell proliferation, which was independent of pancreatic location and circulating factors such as glucose. Identification of the signals responsible for the proliferation of adult, terminally differentiated ß cells will improve strategies aimed at ß cell regeneration and expansion. Overall design: Examination of RNA profiles from isolated whole islets from RIP-rtTA; TetO-VEGF-A mice with no doxycycline (Dox) treatment (3 samples) and after 1 week of Dox (3 sample); and islet-derived macrophages (3 samples) and endothelial cells (3 samples) isolated from dispersed purified islets from RIP-rtTA; TetO-VEGF-A mice after 1 week Dox treatment by fluorescence-activated cell sorting using antibodies against CD11b and CD31, respectively.
Vascular endothelial growth factor coordinates islet innervation via vascular scaffolding.
Specimen part, Cell line, Treatment, Subject
View SamplesBovine papillomavirus (BPV) is the causative agent of papillomatosis in cattle. The disease causes cutaneous and mucosal lesions that can be minimized or lead to the appearance of malignant tumors. This study aims to identify possible molecular mechanisms that are behind the pathological processes associated with bovine papillomatosis through the identification of genes related to the development of the lesions. For this, next-generation RNA sequencing was used to assess differentially expressed genes in infected by BPV and non-infected bovines. Three animals with papillomatosis lesion and three without papillomatosis lesion were studied. The Galaxy platform was used to analyze the data generated by the sequencing. The Illumina output files were converted to FASTQ format. Quality evaluation was performed using FastQC and the sequence quality cut was performed using Trimmomatic. TopHat and Bowtie were used to map and align the reads with the reference genome. The abundance of the expressed genes was verified using Cuffilinks. Cuffdiff was used for differential expression analysis. Functional annotation of the differentially expressed genes was performed using Gene Ontology (GO) databases. RNA-sequencing generated a total of 121,722,238 of reads. In the gene expression analysis, a total of 13,421 genes expressed were identified and of these 1343 were differentially expressed. The functional annotation of differentially significant genes showed that many genes presented functions or they were related to metabolic pathways associated with the progression of papillomatosis lesions and cancer development in cattle. Although more studies are needed, this is the first study that focused on a large-scale evaluation of gene expression associated with the BPV infection, which is important to identify possible mechanisms regulated by the host genes that are necessary the development of the lesion Overall design: Analysis of three BPV infected and three BPV non-infected samples
Comparative transcriptomic analysis of bovine papillomatosis.
Age, Specimen part, Treatment, Subject
View Samples