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A Drosophila proto-oncogene homolog controls aggression via aminergic neurons

ABSTRACT: A Drosophila proto-oncogene homolog controls aggression via aminergic neurons

PROVIDER: PRJNA625242 | ENA |

REPOSITORIES: ENA

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A Drosophila proto-oncogene homolog controls aggression via aminergic neurons

Project description:Modulation of action choices according to the environmental context is crucial for animal survival and reproductive success1. Aggression, despite its general importance as a social behavior2, can become detrimental if uncontrolled3,4. However, the genetic and neural basis for aggression control through active suppression remains largely unknown. Here we found nvy, a Drosophila homolog of vertebrate myeloid translocation gene (MTG)5 involved in transcriptional regulation6-8, suppresses aggression through a specific subset of neurons. Mutation of the nvy gene resulted in hyper-aggressiveness, which was rescued by neuronal expression of human MTGs as well as Drosophila nvy. The mutant exhibited persistent aggression under various contexts in which wild-type flies switch their behavioral patterns. Knockdown of nvy in octopaminergic/tyraminergic (OA/TA) neurons increased aggression, phenocopying the nvy deletion. Cell-type specific transcriptomics on OA/TA neurons derived from the nvy mutants revealed aggression-controlling genes that are likely downstream of nvy. Moreover, we found that the nvy-expressing OA/TA neuronal subpopulations specifically suppress aggression. Our results presents a powerful genetic model to unravel not only the neuronal systems that modulate aggression in a social context-dependent manner, but also the conserved molecular mechanism underlying the tumorigenesis caused by the MTG mutations.

2022-06-22 | GSE148630 | GEO

The proto-oncogene DEK regulates neuronal excitability and tau accumulation in Alzheimer’s disease vulnerable neurons [chromatin]

Project description:Neurons from layer II of the entorhinal cortex (ECII) are the first to accumulate tau protein aggregates and degenerate during prodromal Alzheimer’s disease. We used a data-driven functional genomics approach to model ECII neurons in silico that led us to the prediction that the proto-oncogene DEK is a driver of tau pathology in these neurons. In order to understand the function of DEK in vulnerable neurons, we modulated its expression in ECII neurons in vitro and in vivo in the mouse. Since DEK is a chromatin modulator, we investigated the genomic location of a few histone marks in DEK silenced cells using the CUT&TAG approach, as well as Chromatin Accessibility using ATAC-seq

2022-05-22 | GSE203364 | GEO

The LARP1 homolog Slr1p controls the stability and expression of proto-5’TOP mRNAs in fission yeast [RIP-seq]

Project description:Messenger RNAs (mRNAs) in higher eukaryotes that encode highly expressed proteins important for the assembly of the translational apparatus (e.g. ribosomal proteins) often harbour a pyrimidine-rich motif at the extreme 5’ end known as a 5’ terminal oligopyrimidine (5’TOP) sequence. Members of the La-related protein 1 (LARP1) family control 5’TOP expression through a conserved DM15 motif, but the mechanism is not well understood. 5’TOP motifs have not been described in many lower organisms, but fission yeast (and many other single-celled eukaryotes) harbour a LARP1 homolog that also lacks a DM15 motif. In this work, we show that the fission yeast LARP1 homolog, Slr1p, controls the translation and stability of mRNAs encoding proteins analogous to 5’TOP mRNAs in higher eukaryotes, which we thus refer to as proto-5’TOPs. Our data suggest that the LARP1 DM15 motif and the mRNA 5’TOP motif may be features that were scaffolded over a more fundamental mechanism of LARP1 family member-associated control of gene expression that is still utilized in lower systems.

2023-07-18 | GSE237526 | GEO

The LARP1 homolog Slr1p controls the stability and expression of proto-5’TOP mRNAs in fission yeast [RNA-seq]

2023-07-21 | GSE237860 | GEO

The proto-oncogene DEK regulates neuronal excitability and tau accumulation in Alzheimer’s disease vulnerable neurons [RNA-seq_invivo]

Project description:Neurons from layer II of the entorhinal cortex (ECII) are the first to accumulate tau protein aggregates and degenerate during prodromal Alzheimer’s disease. We used a data-driven functional genomics approach to model ECII neurons in silico that led us to the prediction that the proto-oncogene DEK is a driver of tau pathology in these neurons. In order to understand the function of DEK in vulnerable neurons, we modulated its expression in ECII neurons in vitro and in vivo in the mouse. The present GEO entry corresponds to cell-type specific RNA-sequencing of ECII neurons in vivo 1 week after DEK silencing using AAV vectors.

2022-05-22 | GSE203366 | GEO

The proto-oncogene DEK regulates neuronal excitability and tau accumulation in Alzheimer’s disease vulnerable neurons [RNA-seq_invitro]

Project description:Neurons from layer II of the entorhinal cortex (ECII) are the first to accumulate tau protein aggregates and degenerate during prodromal Alzheimer’s disease. We used a data-driven functional genomics approach to model ECII neurons in silico that led us to the prediction that the proto-oncogene DEK is a driver of tau pathology in these neurons. In order to understand the function of DEK in vulnerable neurons, we modulated its expression in ECII neurons in vitro and in vivo in the mouse. The present GEO entry includes all of the data we collected from DEK-silenced and DEK-overexpressing ECneurons in vitro and in vivo.

2022-05-22 | GSE203365 | GEO

GATA-3 is a proto-oncogene in T-cell lymphoproliferative neoplasms.

Project description:GATA-3 is a proto-oncogene in T-cell lymphoproliferative neoplasms.

| PRJNA832809 | ENA

The proto-oncogene DEK regulates neuronal excitability and tau accumulation in Alzheimer’s disease vulnerable neurons.

Project description:The proto-oncogene DEK regulates neuronal excitability and tau accumulation in Alzheimer’s disease vulnerable neurons.

| PRJNA839693 | ENA

The proto-oncogene DEK regulates neuronal excitability and tau accumulation in Alzheimer’s disease vulnerable neurons [chromatin]

Project description:The proto-oncogene DEK regulates neuronal excitability and tau accumulation in Alzheimer’s disease vulnerable neurons [chromatin]

| PRJNA839697 | ENA

The proto-oncogene TCL1A deregulates mitotic checkpoint transition and genomic stability in CLL

Project description:Upregulation of the proto-oncogene TCL1A is causally implicated in various B- and T-cell malignancies. High-level TCL1A correlates with aggressive disease features and inferior clinical outcomes. However, molecular and cell-biological consequences of TCL1A dysregulation are not fully elucidated. Here, we identify CDC20 and other molecules of the safeguarding cell cycle checkpoints as novel TCL1A-interactors. In different model systems of B-cell leukemia/lymphoma, TCL1A overexpression accelerated cell cycle transition, impaired apoptotic damage responses in association with pronounced chromosome mis-segregation and caused cellular aneuploidy. In primary CLL samples, low CDC20 expression correlated with high expression of TCL1A and more aggressive disease characteristics. In line, a low CDC20 expression was a marker for reduced progression-free survival in CLL patients. Finally, knockdown of CDC20 in TCL1A-initiated murine lymphomas promoted chromosome disbalances and leukemia outgrowth. Overall, we discovered a cell-cycle associated effect of TCL1A by interfering with a proficient cell cycle transition. This adds to our concept of TCL1A’s transforming impact by targeting genome stability.

2022-11-14 | PXD030776 | Pride

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