Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

FtsH12 abundance modulates chloroplast development in Arabidopsis thalian

ABSTRACT: Proteomic investigation of Arabidopsis thaliana ftsH12 - ftsH12 is one of 17 genes of the FtsH metallo-protease family encoded within the A. thaliana genome.

INSTRUMENT(S): maXis

ORGANISM(S): Arabidopsis Thaliana (mouse-ear Cress)

TISSUE(S): Plant Cell, Leaf, Rosette

SUBMITTER: Fatih Demir

LAB HEAD: Pitter Florian Huesgen

PROVIDER: PXD010615 | Pride | 2020-11-25

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	180216AthCol-0mycA_RA1_01_4293.d.zip	Other
	180216AthFtsH12mycHisA_BH12_01_4292.d.zip	Other
	180216AthFtsH12mycmycA_BH5_01_4277.d.zip	Other
	180220AthCol-0mycB_RB6_01_4328.d.zip	Other
	180220AthFtsH12mycHisB_RB4_01_4326.d.zip	Other

Items per page:

1 - 5 of 7

Publications

Abundance of metalloprotease FtsH12 modulates chloroplast development in Arabidopsis thaliana.

Mielke Kati K Wagner Raik R Mishra Laxmi S LS Demir Fatih F Perrar Andreas A Huesgen Pitter F PF Funk Christiane C

Journal of experimental botany 20210401 9

The ATP-dependent metalloprotease FtsH12 (filamentation temperature sensitive protein H 12) has been suggested to participate in a heteromeric motor complex, driving protein translocation into the chloroplast. FtsH12 was immuno-detected in proplastids, seedlings, leaves, and roots. Expression of Myc-tagged FtsH12 under its native promotor allowed identification of FtsHi1, 2, 4, and 5, and plastidic NAD-malate dehydrogenase, five of the six interaction partners in the suggested import motor compl ...[more]

PMID: 33216923

Similar Datasets

A unique iron homeostasis regulatory circuit with reciprocal roles in Candida albicans commensalism and pathogenesis [ChIP_chip]

Project description:The mammalian gastrointestinal tract and the bloodstream are highly disparate biological niches, and yet certain commensal-pathogenic microorganisms are able to thrive in both environments. Here, we report the evolution of a unique transcription circuit in the yeast, Candida albicans, which determines its fitness in both host niches. Our comprehensive analysis of the DNA-binding proteins that regulate iron uptake by this organism suggests the evolutionary intercalation of a transcriptional activator called Sef1 between two broadly conserved transcriptional repressors, Sfu1 and Hap43. The Sef1 activator of iron uptake genes promotes virulence in a mouse model of bloodstream infection, whereas the Sfu1 repressor is dispensable for virulence but promotes gastrointestinal commensalism. We propose that the ability to alternate between genetic programs conferring resistance to iron depletion in the bloodstream versus iron toxicity in the gut may be a fundamental attribute of gastrointestinal commensal-pathogens. ChIP analyses to profile genome-wide of distribution of Sef1, Sfu1 and Hap43 in response to various iron availability. 12 independent ChIP experiments were performed on 6 biological replicates of the untagged control and 2 biological replicates each of Sef1-Myc, Sfu1-Myc, and Hap43-Myc.

2011-07-12 | E-GEOD-30591 | biostudies-arrayexpress

Dynamics of replication-independent histone turnover in budding yeast

Project description:This SuperSeries is composed of the following subset Series: GSE6664: Ratios for unsync cells GSE6665: Ratios for G1 arrested cells (Printed array) GSE6666: Ratios for G1 arrested cells (Agilent array) GSE6667: PolII occupancy GSE6668: Nucleosome occupancy GSE6669: H3 occupancy GSE6670: Ratios for Htz1D cells (Agilent array) Keywords: SuperSeries Refer to individual Series

2010-06-11 | E-GEOD-6680 | biostudies-arrayexpress

H3 occupancy

Project description:Chromatin plays roles in processes governed by different time scales. To assay the dynamic behaviour of chromatin in living cells, we used genomic tiling arrays to measure histone H3 turnover in G1-arrested S. cerevisiae at single-nucleosome resolution over 4% of the genome, and over the entire genome at lower (~265 bp) resolution. We find that nucleosomes at promoters are replaced more rapidly than at coding regions, and that replacement rates over coding regions correlate with polymerase density. In addition, rapid histone turnover is found at known chromatin boundary elements. These results suggest that rapid histone turnover serves to functionally separate chromatin domains and prevent spread of histone states. Keywords: Chip-chip, H3 ChIP-chip for Myc-H3 vs WCE.

2007-05-16 | E-GEOD-6669 | biostudies-arrayexpress

Ratios for G1 arrested cells (Printed array)

2010-06-11 | E-GEOD-6665 | biostudies-arrayexpress

Arabidopsis thaliana ftsH12 label-free shotgun

Project description:Proteomic investigation of Arabidopsis thaliana ftsH12 - ftsH12 is one of 17 genes of the FtsH metallo-protease family encoded within the A. thaliana genome.

2020-11-09 | PXD010619 | Pride

Identification of WRKY22 direct targets under submergence in Arabidopsis with ChIP

Project description:To identify direct targets of WRKY22, we created a transgenic Arabidopsis line that expresses a c-myc epitope-tagged WRKY22 and used ChIP followed by microarray hybridization (ChIP-chip) to screen for candidates and validate the in vivo protein-DNA interactions with ChIP followed by quantitative PCR (ChIP-Q-PCR). The WRKY22 and c-myc epitope tag fusion construct was generated and transformed into wrky22-ko2 plants. The resulting transgenic lines should have better ChIP efficiency than the wild-type background, due to the reduced competition for WRKY22 binding sites from endogenous WRKY22. ChIP-enriched DNA fragments were identified using criteria of a window of +300 to M-oM-<M-1200 of a gene for a promoter, a width of 4 probes or more, and a false discovery rate (FDR) < 0.1. The ChIP-chip experiments were repeated six times, i.e., six biological replicas. Candidates were defined by the presence of the promoter in three out of six biological replicas. Candidates were then classified based on their hypoxic responsiveness with a positive response defined as gene expression levels exhibiting > 2 or < 0.5-fold induction in any time point under submergence treatments in expression array data. Comparison of c-myc tagged WRKY22 transgenic plants vs wild-type (Columbia) plants. Both materials were submergence treated for 3 hours.

2013-07-03 | E-GEOD-40138 | biostudies-arrayexpress

The phosphatase DUSP22/JKAP inhibits UBR2-mediated K63-ubiquitination and activation of Lck in TCR signaling

Project description:DUSP22 (also named JKAP) is a dual-specificity phosphatase that inhibits T cell activation. Here we identified the E3 ubiquitin ligase UBR2 as an upstream activator of Lck during T-cell activation. JKAP dephosphorylated UBR2 at two residues, leading to ubiquitin-mediated UBR2 degradation. The SCF (SKP1-CUL1-βTrCP) complex induced UBR2 Lys48-linked ubiquitination at three lysine residues. Moreover, single-cell RNA sequencing analysis and UBR2 knockout showed that UBR2 increased proinflammatory cytokines. Remarkably, UBR2 induced Lys63-linked ubiquitination of Lck at two lysine residues and subsequent Lck Tyr394 phosphorylation/activation in TCR signaling. Conversely, TCR-induced Lck activation and JKAP knockout-enhanced inflammatory phenotypes were attenuated by UBR2 knockout. Consistently, the UBR2- Lck interaction and Lck Lys63-linked ubiquitination were induced in peripheral blood T cells of human SLE patients. Collectively, UBR2 protein stability and UBR2-induced Lck ubiquitination/activation are inhibited by JKAP, leading to attenuation of T-cell activation and T-cell-mediated inflammation.

2024-01-04 | PXD043490 | Pride

The phosphatase DUSP22/JKAP inhibits UBR2-mediated K63-ubiquitination and activation of Lck in TCR signaling

2024-01-04 | PXD043463 | Pride

The phosphatase DUSP22/JKAP inhibits UBR2-mediated K63-ubiquitination and activation of Lck in TCR signaling ( Sequential regulation of Lck K63-ubiquitination and autophosphorylation by UBR2 and DUSP22/JKAP in TCR signaling)

Project description:DUSP22 (also named JKAP) is a dual-specificity phosphatase that inhibits T cell activation. Here we identified the E3 ubiquitin ligase UBR2 as an upstream activator of Lck during T-cell activation. JKAP dephosphorylated UBR2 at two residues, leading to ubiquitin-mediated UBR2 degradation. The SCF (SKP1-CUL1-βTrCP) complex induced UBR2 Lys48-linked ubiquitination at three lysine residues. Moreover, single-cell RNA sequencing analysis and UBR2 knockout showed that UBR2 increased proinflammatory cytokines. Remarkably, UBR2 induced Lys63-linked ubiquitination of Lck at two lysine residues and subsequent Lck Tyr394phosphorylation/activation in TCR signaling. Conversely, TCR-induced Lck activation and JKAP knockout-enhanced inflammatory phenotypes were attenuated by UBR2 knockout. Consistently, the UBR2-Lck interaction and Lck Lys63-linked ubiquitination were induced in peripheral blood T cells of human SLE patients. Collectively, UBR2 protein stability and UBR2-induced Lck ubiquitination/activation are inhibited by JKAP, leading to attenuation of T-cell activation and T-cell-mediated inflammation.

2024-01-04 | PXD043454 | Pride

Telomerase subunit TERT regulates MYC stability independent of its role on telomeres (ChIP-Seq)

Project description:Constitutively active MYC and reactivated telomerase often co-exist in cancers. While the reactivation of telomerase is thought to be essential for replicative immortality, MYC, in conjunction with co-factors, confers several growth advantages to cancer cells. However, it is unclear which co-factors sustain elevated MYC activity in tumours . Here, we identify TERT, the catalytic subunit of telomerase, as a novel regulator of MYC stability in cancers. Binding of TERT to MYC stabilizes its levels on chromatin, contributing to either activation or repression of its target genes. Mechanistically, TERT regulates MYC ubiquitination and stability, and this effect of TERT is independent of its role on telomeres. Genetic inhibition and knocking out of TERT phenocopied the loss of MYC, resulting in reduced disease burden of early- and late-stage MYC-driven murine lymphomas. Conversly, the ectopic expression of TERT could substitute for reduced MYC in these functions. Finally we show that TERT null mice, unlike Terc null mice, show delayed onset of MYC induced lymphomagenesis. Accordingly, inhibiting TERT function in primary human leukemia cells blocked the expression of MYC targets, while Terc depletion had no effects . Based on our data, we conclude that the re-expression of TERT, a direct MYC target in tumors, provides a feed-forward mechanism to potentiate MYC-dependent oncogenesis. ChIP was performed using anti-MYC (sc-764) in primary lymphoma cells from Eµ-Myc;Tert -/- mice, Eµ-Myc;Tert +/+ mice, or in P493 cells treated with shTert, P493 shTerc and shControl.

2015-04-23 | E-GEOD-60223 | biostudies-arrayexpress