Massive bursts of TE activity in Drosophila
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR557048_1.fastq.gz | Fastqsanger.gz | |||
| ERR557048_2.fastq.gz | Fastqsanger.gz | |||
| ERR557049_1.fastq.gz | Fastqsanger.gz | |||
| ERR557049_2.fastq.gz | Fastqsanger.gz | |||
| ERR557050_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 40 |
Similar Datasets
Project description:Respiratory bursts were observed in A. bisporus. CO2 production and O2 consumption increased up to 3.5 fold during these 3 h bursts while compost temperature increased up to 3 °C. We set out to find which pathways were characteristic for these bursts and the interval between these bursts.
2021-02-24 | GSE124976 | GEO
Project description:Agaricus bisporus respiratory bursts
| PRJNA514729 | ENA
Project description:Somatic mutations and transposable element (TE) dysregulation are hallmarks of cancer, yet how specific genetic alterations influence TE activity across tumor types remains unclear. Here, we mapped mutation–TE regulatory networks across 9,622 tumors representing 33 TCGA cancer types by integrating RNA-seq, whole-exome, and DNA methylation data. Comparative analysis of tumors with and without mutations identified 275 significant cancer–gene pairs associated with altered TE expression, many of which are transcription factors such as TP53, NSD1 and ARID1A. The changes in TE expression were also inversely correlated with DNA methylation changes in many cases. Unexpectedly, we observed that immune pathway activity is down-regulated when TE expression is induced, and up-regulated when TE is repressed. Functional validation in isogenic ARID1A- and CTNNB1-perturbed models recapitulated the changes in TE activity and immune responses observed in TCGA datasets. Together, these findings reveal mutation-driven TE activity reprogramming as a widespread feature and a potential source for immune modulation in human cancers.
2026-04-01 | GSE320262 | GEO
Project description:Somatic mutations and transposable element (TE) dysregulation are hallmarks of cancer, yet how specific genetic alterations influence TE activity across tumor types remains unclear. Here, we mapped mutation–TE regulatory networks across 9,622 tumors representing 33 TCGA cancer types by integrating RNA-seq, whole-exome, and DNA methylation data. Comparative analysis of tumors with and without mutations identified 275 significant cancer–gene pairs associated with altered TE expression, many of which are transcription factors such as TP53, NSD1 and ARID1A. The changes in TE expression were also inversely correlated with DNA methylation changes in many cases. Unexpectedly, we observed that immune pathway activity is down-regulated when TE expression is induced, and up-regulated when TE is repressed. Functional validation in isogenic ARID1A- and CTNNB1-perturbed models recapitulated the changes in TE activity and immune responses observed in TCGA datasets. Together, these findings reveal mutation-driven TE activity reprogramming as a widespread feature and a potential source for immune modulation in human cancers.
2026-04-01 | GSE320261 | GEO
Project description:Somatic mutations and transposable element (TE) dysregulation are hallmarks of cancer, yet how specific genetic alterations influence TE activity across tumor types remains unclear. Here, we mapped mutation–TE regulatory networks across 9,622 tumors representing 33 TCGA cancer types by integrating RNA-seq, whole-exome, and DNA methylation data. Comparative analysis of tumors with and without mutations identified 275 significant cancer–gene pairs associated with altered TE expression, many of which are transcription factors such as TP53, NSD1 and ARID1A. The changes in TE expression were also inversely correlated with DNA methylation changes in many cases. Unexpectedly, we observed that immune pathway activity is down-regulated when TE expression is induced, and up-regulated when TE is repressed. Functional validation in isogenic ARID1A- and CTNNB1-perturbed models recapitulated the changes in TE activity and immune responses observed in TCGA datasets. Together, these findings reveal mutation-driven TE activity reprogramming as a widespread feature and a potential source for immune modulation in human cancers.
2026-04-01 | GSE320258 | GEO
Project description:Somatic mutations and transposable element (TE) dysregulation are hallmarks of cancer, yet how specific genetic alterations influence TE activity across tumor types remains unclear. Here, we mapped mutation–TE regulatory networks across 9,622 tumors representing 33 TCGA cancer types by integrating RNA-seq, whole-exome, and DNA methylation data. Comparative analysis of tumors with and without mutations identified 275 significant cancer–gene pairs associated with altered TE expression, many of which are transcription factors such as TP53, NSD1 and ARID1A. The changes in TE expression were also inversely correlated with DNA methylation changes in many cases. Unexpectedly, we observed that immune pathway activity is down-regulated when TE expression is induced, and up-regulated when TE is repressed. Functional validation in isogenic ARID1A- and CTNNB1-perturbed models recapitulated the changes in TE activity and immune responses observed in TCGA datasets. Together, these findings reveal mutation-driven TE activity reprogramming as a widespread feature and a potential source for immune modulation in human cancers.
2026-04-01 | GSE320255 | GEO
Project description:Changes in cell morphology require the dynamic remodeling of the actin cytoskeleton. Calcium fluxes have been suggested as an important signal to rapidly relay information to the actin cytoskeleton, but the underlying mechanisms remain poorly understood. Here, we identify the EF-hand domain containing protein EFhD2/Swip-1 as a conserved lamellipodial protein strongly upregulated in Drosophila macrophages at the onset of metamorphosis when macrophage behavior shifts from quiescent to migratory state. Loss- and gain-of-function analysis confirm a critical function of EFhD2/Swip-1 in lamellipodial cell migration in fly and mouse melanoma cells. Contrary to previous assumptions, TIRF-analyses unambiguously demonstrate that EFhD2/Swip-1 proteins efficiently cross-link actin filaments in a calcium-dependent manner. Using a single-cell wounding model, we show that EFhD2/Swip-1 promotes wound closure in a calcium-dependent manner. Mechanistically, our data suggest that transient calcium bursts reduce EFhD2/Swip-1 cross-linking activity and thereby promote rapid reorganization of existing actin networks to drive epithelial wound closure.
2022-04-19 | GSE200966 | GEO
Project description:Sporosarcina sp. Te-1 Genome sequencing
| PRJNA713852 | ENA
Project description:Antibody affinity maturation occurs in secondary lymphoid organs within germinal centers (GCs) where B cells mutate their antibody-encoding genes in the dark zone (DZ) followed by a selection of the high-affinity variants in the light zone (LZ) by T cells. The amount of the T cell-derived selection signals is proportional to the BCR affinity and the magnitude of Myc expression. However, since the lifetimes of Myc mRNA and protein are extremely short, it is unclear how high levels of Myc are maintained in the GC B cell to allow positive selection. Here, by measuring Myc transcripts in situ at the single-cell level, we find that T cell help promotes the frequency of Myc transcriptional bursts. T cell help primarily increases the number of Myc-positive cells rather than the amount of Myc per cell. Measurement of Myc intronic and exonic transcripts in situ demonstrates that positive selection is mediated by Myc transcriptional bursts through a rapid increase in the active transcription sites rather than an elevation in transcription rate or gene accessibility. Thus, the amount of Myc transcriptional bursts over time in the LZ, rather than Myc abundance, dictates B cell selection in germinal centers.
2024-10-15 | GSE237128 | GEO
Project description:TE-Array is a custom Agilent microarray that probes for transposable elements in both sense and antisense orientations in humans and mice. TE-Array was used to study expression levels of transposable elements (TE) in a panel of normal mouse tissues. TE-Array comprises of 4 different custom Agilent 4X44K designs. These 4 different designs have probes for human sense orientation, human antisense orientation, mouse sense orientation and mouse antisense orientation transposable elements. These array designs were used to study the transposon abundance profile in 7 different mouse tissue samples, 2 mouse cell lines and 1 transposon transfected versus untransfected human cell line.
2013-11-16 | E-GEOD-52412 | biostudies-arrayexpress