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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Profiling of Lola-N genomic binding in Drosophila with DamID

ABSTRACT: The ability to reprogram differentiated cells into a pluripotent state has revealed that the differentiated state is plastic and reversible. It is evident, therefore, that mechanisms must be in place to maintain cells in a differentiated state. Transcription factors that specify neuronal characteristics have been well studied but less is known about the mechanisms that prevent neurons from dedifferentiating to a multipotent, stem cell-like state. Here we identify Lola as a transcription factor that is required to maintain neurons in a differentiated state. We show that Lola represses neural stem cell genes and cell cycle genes in post-mitotic neurons. In lola mutants, neurons dedifferentiate, turn on neural stem cell genes and begin to divide, forming tumours. Thus, neurons rather than stem cells or intermediate progenitors are the tumour-initiating cells in lola mutants. 3 biological relicates were performed for Lola-N (with one dye-swap).

ORGANISM(S): Drosophila melanogaster

SUBMITTER: Tony Southall

PROVIDER: E-GEOD-53447 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Profiling of Lola-N genomic binding in Drosophila with DamID

Project description:The ability to reprogram differentiated cells into a pluripotent state has revealed that the differentiated state is plastic and reversible. It is evident, therefore, that mechanisms must be in place to maintain cells in a differentiated state. Transcription factors that specify neuronal characteristics have been well studied but less is known about the mechanisms that prevent neurons from dedifferentiating to a multipotent, stem cell-like state. Here we identify Lola as a transcription factor that is required to maintain neurons in a differentiated state. We show that Lola represses neural stem cell genes and cell cycle genes in post-mitotic neurons. In lola mutants, neurons dedifferentiate, turn on neural stem cell genes and begin to divide, forming tumours. Thus, neurons rather than stem cells or intermediate progenitors are the tumour-initiating cells in lola mutants.

2014-05-06 | GSE53447 | GEO

Profiling of Esg genomic binding in the Drosophila midgut with DamID

Project description:Tissue stem cells divide asymmetrically to self-renew and generate differentiated progeny to maintain tissue homeostasis. Escargot (Esg) is a transcriptional repressor that is expressed in multiple stem cell populations in Drosophila melanogaster. Reduced esg function in intestinal stem cells (ISCs) causes a loss of ISCs and a biased differentiation of the daughter enteroblasts (EBs) toward the enteroendocrine (EE) cell fate. Loss of esg leads to an upregulation of differentiation factors and reduced Notch activity within EBs, indicating that Esg is a pivotal regulator of homeostasis in the intestine, supporting self-renewal to maintain a healthy stem cell pool as well as differentiation of progenitor cells. To identify potential transcriptional targets that mediate these phenotypes, in vivo DamID was used to generate the data deposited herein. 3 biological relicates were performed for Esg (with one dye-swap).

2014-11-18 | E-GEOD-55226 | biostudies-arrayexpress

Profiling of Islet, Lim3, Hb9 and Eve genomic binding in Drosophila with DamID

Project description:While developmental processes such as axon pathfinding and synapse formation have been characterized in detail, comparatively less is known of the intrinsic developmental mechanisms that regulate transcription of ion channel genes in embryonic neurons. Early decisions, including motoneuron axon targeting, are orchestrated by a cohort of transcription factors that act together in a combinatorial manner. These transcription factors include Even-skipped (Eve), Islet, Lim3 and Hb9. The perdurance of these factors in late embryonic neurons is, however, indicative that they might also regulate additional aspects of neuron development, including the acquisition of electrical properties. We have shown that Eve binds and regulates both voltage- and ligand-gated currents in motoneurons (Pym et al., 2006). We have also shown that Islet is sufficient to repress a Shaker-mediated A-type K(+) current, most likely due to a direct transcriptional effect (Wolfram et al., 2012). Finally, we have shown that Islet and Lim3 act in a combinatorial fashion to regulate Shaker-mediated A-type K(+) current (Wolfram et al., 2014). 3 biological relicates were performed for Islet, Lim3 and Hb9 (with one dye-swap). 2 biological relicates were performed for Eve.

2014-02-18 | E-GEOD-53446 | biostudies-arrayexpress

DamID profiling of neural transcription factor (Abrupt and Knot) binding in Drosophila melanogaster embryos

Project description:Paper abstract: The transcription factors Abrupt (Ab) and Knot (Kn) act as selectors of distinct dendritic arbor morphologies in two classes of Drosophila sensory neurons, termed class I and class IV, respectively. We performed binding-site mapping and transcriptional profiling of isolated these neurons. Their profiles were similarly enriched in cell-type-specific enhancers of genes implicated in neural development. We identified a total of 429 target genes, of which 56 were common to Ab and Kn; these targets included genes necessary to shape dendritic arbors in either or both of the two sensory subtypes. Furthermore, a common target gene, encoding the cell adhesion molecule Ten-m, was expressed more strongly in class I than IV, and this differential was critical to the class-selective directional control of dendritic branch sprouting or extension. Our analyses illustrate how differentiating neurons employ distinct and shared repertoires of gene expression to produce class-selective morphological traits. Each Dam-fusion-derived sample is compared to a control Dam-only sample. Four biological replicates were performed.

2013-11-27 | E-GEOD-38659 | biostudies-arrayexpress

lola-PI-GFP_W3L_ChIP-seq

Project description:modENCODE_submission_5003 This submission comes from a modENCODE project of Kevin White. For full list of modENCODE projects, see http://www.genome.gov/26524648 Project Goal: The White Lab is aiming to map the association of all the Transcription Factors (TF) on the genome of Drosophila melanogaster. One technique that we use for this purpose is chromatin immunoprecipitation coupled with deep sequencing (ChIP-seq) utilizing an Illumina next generation sequencing platform. The data generated by ChIP-seq experiments consist basically of a plot of signal intensity across the genome. The highest signals correspond to positions in the genome occupied by the tested TF. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf EXPERIMENT TYPE: CHIP-seq. BIOLOGICAL SOURCE: Strain: lola-RI-GFP; Developmental Stage: L3; Genotype: PBac{y[+]-attP-3B}VK00033; Sex: Unknown; Transgene: lola-RI genomic coding region; EXPERIMENTAL FACTORS: Developmental Stage L3; Target gene lola; Strain lola-RI-GFP; Antibody GFP ab290 (target is Green Fluorescent Protein)

2013-08-28 | E-GEOD-50372 | biostudies-arrayexpress

Roles of Lola-O

Project description:Roles of Lola-O

| PRJNA404083 | ENA

RNA-Sequencing of Wild Type, Lola-F and Lola-Null mutant embryos

Project description:longitudinals lacking (lola) is among the most complex genes in Drosophila melanogaster, encoding up to 20 different protein isoforms and acting as a key transcription factor in axonal pathfinding and neural reprograming. To better characterize Lola function we have generated specific mutations in each isoform using the CRISPR/Cas9 system. Our targeted screen allows us to revisit the previously demonstrated roles for few isoforms, to assign known functions to specific isoforms and to reveal a critical role for a specific variant in the octopaminergic pathway. Thus, our comprehensive study expands the repertoire of Lola functions, and demonstrates that the CRISPR/Cas9 approach is a valuable tool to systematically address the role of complex loci in vivo.

2020-01-08 | GSE93294 | GEO

lola-PJ-GFP_0-12h_embryo_ChIP-seq

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2013-08-11 | E-GEOD-49772 | biostudies-arrayexpress

lola-PJ-GFP_12-24h_embryo_ChIP-seq

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2013-08-11 | E-GEOD-49773 | biostudies-arrayexpress

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