Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

NWU Study 3- SLAM-seq timecourse of KOLF2.2J hiPSC after Auxin-induced protein degradation of specific gene products

ABSTRACT: This study investigates the impact of gene products on nscent transcription in growing hiPSC at 0, 6 & 24 hours after acute protein depletion. Crispr editing was used to add an auxin-dependent degron to the C-termini of gene products expressed from the endogeneous loci and to insert an auxin-responsive degradation E3 ligase to the AAVS locus. Rapid (<30 min), specific target protein degradation in KOLF2.2J hiPSCs was induced by a synthetic auxin derivative (5-Ad-IAA) and bulk ATAC-seq was performed at timepoints to define early (6 hr) and later (24 hr) downstream transcriptional dependencies.

ORGANISM(S): Homo sapiens

PROVIDER: GSE346716 | GEO | 2026/09/12

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

NWU Study 2- ATAC-seq timecourse of KOLF2.2J hiPSC after Auxin-induced protein degradation of specific gene products

Project description:This study investigates the impact of gene products on chromatin accessibility in growing hiPSC at 0, 6 & 24 hours after acute protein depletion. Crispr editing was used to add an auxin-dependent degron to the C-termini of gene products expressed from the endogeneous loci and to insert an auxin-responsive degradation E3 ligase to the AAVS locus. Rapid (<30 min), specific target protein degradation in KOLF2.2J hiPSCs was induced by a synthetic auxin derivative (5-Ad-IAA) and bulk ATAC-seq was performed at timepoints to define early (6 hr) and later (24 hr) downstream chromatin remodeling.

2026-08-12 | GSE343368 | GEO

NWU Study 1- Bulk RNA seq timecourse of KOLF2.2J hiPSC after Auxin-induced protein degradation of specific gene products

Project description:This study investigates the impact of 2 gene products (RBBP4, CHD1) on transcriptional programming in growing hiPSC at 0, 6 & 24 hours after acute protein depletion. Crispr editing was used to add an auxin-dependent degron to the C-termini of gene products expressed from the endogeneous loci and to insert an auxin-responsive degradation E3 ligase to the AAVS locus. Rapid (<30 min), specific target protein degradation in KOLF2.2J hiPSCs was induced by a synthetic auxin derivative (5-Ad-IAA) and bulk RNA-seq was performed at timepoints to define early (6 hr) and later (24 hr) downstream transcriptional dependencies.

2025-02-03 | GSE288398 | GEO

Homo sapiens

Project description:time 24 hr to 0 hr

| PRJNA89813 | ENA

Structure, function and microbial ecology of diverse MarR bacterial regulators of auxin catabolism

Project description:Chemical signaling in the plant microbiome can have drastic effects on microbial community structure, and on host growth and development. Previously, we demonstrated that the auxin metabolic signal interference performed by the bacterial genus Variovorax via a novel auxin degradation locus was essential for maintaining stereotypic root development in an ecologically-relevant bacterial synthetic community. Here, we dissect the Variovorax auxin degradation locus to define the genes necessary and sufficient for indole-3-acetic acid (IAA) degradation and signal interference. We determine the crystal structures and binding properties of the operon’s MarR-family repressor with IAA and other auxins. We identify auxin-degradation operons across the bacterial tree of life and define two distinct types based on gene content and metabolic products: iac-like and iad-like. We solve the structures of MarRs from representatives of each auxin degradation operon type, establishing that each have distinct IAA binding pockets. Comparison of representative IAA degrading strains from diverse bacterial genera show that while all degrade IAA, only strains containing iad-like auxin degrading operons interfere with auxin signaling in a complex synthetic community context. This suggests that iad-like operon containing strains, including Variovorax species, play a key ecological role in modulating auxins in the plant microbiome.

2022-08-11 | GSE210968 | GEO

SLAM-Seq of UPF1 depletion in human colorectal adenocarcinoma cell line HCT116 via the auxin-inducible degron (AID) system

Project description:UPF1 is a multi-domain RNA helicase that constantly monitors the transcriptome by non-specifically binding to mRNAs, dissociating from non-target transcripts, and initiating degradation on selected target RNAs via multiple proposed pathways such as nonsense-mediated decay (NMD). NMD is a translation-coupled mechanism that targets mRNAs harboring a premature stop codon (PTC) for degradation, thereby serving as a quality control and gene regulatory pathway ensuring transcriptome integrity. The UPF1 gene is essential in cultured human cells and previous studies relied mostly on RNA interference to downregulate UPF1. Here we established an auxin-inducible UPF1 degron system in the human colorectal adenocarcinoma cell line HCT116 by first inserting the auxin receptor F-box protein-encoding AtAFB2-mCherry in the AAVS1 locus, followed by tagging UPF1 at the N-terminus with an V5-AID-tag (AID = miniIAA7 = AtIAA7 amino acids 37–104). Using SLAM-Seq and this cell line, we wanted to explore the time-resolved RNA stability changes upon rapid depletion of UPF1. To this end, depletion of UPF1 was induced with 500 µM indole-3-acetic acid (IAA) for various time periods (0h, 12h and 24h) and the cells were labeled with 200 µM 4-thiouridine (4SU) the last 2 hours before harvesting. As controls, the parental cell line (with AtAFB2-mCherry in the AAVS1 locus) or unlabeled cells were used.

2025-09-01 | E-MTAB-13836 | biostudies-arrayexpress

Loss of protein association causes cardiolipin degradation in Barth syndrome

Project description:Loss of protein association causes cardiolipin degradation in Barth syndrome Dataset1: effect of bromopyruvate EH_011316_Forward1.raw (treated: heavy label; control: medium label) EH_011316_Reverse1.raw (treated: medium label; control: heavy label) Dataset2: Barth versus control cell (Barth cells: heavy label; control cells: medium label) EH_020514_mix24H.raw (24 hr incubation, replicate 1) EH_020514_mix32H.raw (32 hr incubation, replicate 1) EH_020614_mix24H.raw (24 hr incubation, replicate 2) EH_020614_mix32H.raw (32 hr incubation, replicate 2) EH_020714_mix24H.raw (24 hr incubation, replicate 3) EH_020714_mix32H.raw (32 hr incubation, replicate 3)

2016-03-22 | MSV000079599 | MassIVE

Coordination of rhythmic RNA synthesis and degradation orchestrates 24- and 12-h RNA expression patterns in mouse fibroblasts

Project description:Circadian RNA expression is essential to ultimately regulate a plethora of downstream rhythmic biochemical, physiological, and behavioral processes. Both transcriptional and post transcriptional mechanisms are considered important to drive rhythmic RNA expression, however, the extent to which each regulatory process contributes to the rhythmic RNA expression remains controversial. To systematically address this, we monitored RNA dynamics using metabolic RNA labeling technology during a circadian cycle in mouse fibroblasts. We find that rhythmic RNA synthesis is the primary contributor of 24 hr RNA rhythms, while rhythmic degradation is more important for 12 hr RNA rhythms. These rhythms were predominantly regulated by Bmal1 and/or the core clock mechanism, and interplay between rhythmic synthesis and degradation has a significant impact in shaping rhythmic RNA expression patterns. Interestingly, core clock RNAs are regulated by multiple rhythmic processes and have the highest amplitude of synthesis and degradation, presumably critical to sustain robust rhythmicity of cell-autonomous circadian rhythms. Our study yields invaluable insights into the temporal dynamics of both 24 hr and 12 hr RNA rhythms in mouse fibroblasts.

2024-01-22 | GSE253826 | GEO

Auxin-inducible degron 2 system deciphers functions of CTCF domains in transcriptional regulation [SLAM-seq]

Project description:Background: CTCF is a well-established chromatin architectural protein that also plays various roles in transcriptional regulation. While CTCF biology has been extensively studied, how the domains of CTCF function to regulate transcription remains unknown. Additionally, the original auxin-inducible degron 1 (AID1) system has limitations to investigate the function of CTCF. Results: We employ an improved auxin-inducible degron technology, AID2, to facilitate the study of acute depletion of CTCF while overcoming the limitations of the previous AID system. As previously observed through the AID1 system and steady-state RNA analysis, the new AID2 system combined with SLAM-seq confirms that CTCF depletion leads to modest nascent and steady-state transcripts changes. A CTCF domain sgRNA library screening identifies the zinc finger (ZF) domain as the region within CTCF with the most functional relevance, including ZFs 1 and 10. Removal of ZFs 1 and 10 reveals genomic regions that independently require these ZFs for DNA binding and transcriptional regulation. Notably, loci regulated by either ZF1 or ZF10 exhibit unique CTCF binding motifs specific to each ZF. Conclusions: By extensively comparing the AID1 and AID2 systems for CTCF degradation in SEM cells, we confirm that AID2 degradation is superior for achieving miniAID tagged protein degradation without the limitations of the AID1 system. The model we create that combines AID2 depletion of CTCF with exogenous overexpression of CTCF mutants allows us to demonstrate how peripheral ZFs intricately orchestrate transcriptional regulation in a cellular context for the first time.

2022-12-09 | GSE205184 | GEO

CUT&Tag data of MBD3 in mouse embryonic stem cells treated with auxin for CHD4 depletion against untreated control

Project description:This study investigates the effect of the chromatin remodeller CHD4 on MBD3 using CUT&Tag. CHD4 was tagged with a mini-AID degron to enable auxin-inducible degradation. CUT&Tag for MBD3 was performed at multiple time-points (4 hours and 24 hours) following auxin treatment vs untreated control (0 hours) to capture changes in MBD3 binding upon CHD4 depletion. For each time point, two biological replicates were processed.

2026-01-15 | E-MTAB-15627 | biostudies-arrayexpress

CUT&Tag data of H3K27Ac and H3K4Me1 in mouse embryonic stem cells treated with auxin for CHD4 depletion against untreated control

Project description:This study investigates the effect of the chromatin remodeller CHD4 on H3K27Ac and H3K4Me1 using CUT&Tag. CHD4 was tagged with a mini-AID degron to enable auxin-inducible degradation. CUT&Tag for H3K27Ac and H3K4Me1 was performed at multiple time-points (4 hours and 24 hours) following auxin treatment vs untreated control (0 hours) to capture changes in histone modifications upon CHD4 depletion. For each time point, three biological replicates were processed.

2026-01-15 | E-MTAB-15625 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data