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ABSTRACT: DT-DYLC &DT-DYLCJ

PROVIDER: PRJNA1237704 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32752200_1.fastq.gz	Fastqsanger.gz
	SRR32752200_2.fastq.gz	Fastqsanger.gz
	SRR32752201_1.fastq.gz	Fastqsanger.gz
	SRR32752201_2.fastq.gz	Fastqsanger.gz
	SRR32752202_1.fastq.gz	Fastqsanger.gz

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Delftia sp. DT strain:DT | isolate:intestine

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Seed comparative genomics in three coffee species evidence desiccation tolerance mechanisms among intermediate seeds

Project description:In contrast to the desiccation tolerant (DT) ‘orthodox’ seeds, the so-called ‘intermediate’ seeds cannot survive complete drying and are short-lived. All species of the genus Coffea produce intermediate seeds but show a considerable variability for the seed DT level, which may help to decipher the molecular basis of seed DT in plants. We thus led a comparative transcriptome analysis of developing seeds in three coffee species with contrasting seed DT levels. Seeds of all species shared a major transcriptional switch during late maturation that governs a general slow-down of metabolism. However, numerous key stress-related genes, including those coding for the late embryogenesis abundant protein EM6 and the osmosensitive calcium channel ERD4, were upregulated during DT acquisition in the two species with high seed DT, C. arabica and C. eugenioides. By contrast, an upregulation of numerous players of the metabolism, transport and perception of auxin was observed in C. canephora seeds with low DT. Moreover, species with high DT showed a stronger down-regulation of the mitochondrial machinery dedicated to the tricarboxylic acid cycle and oxidative phosphorylation. Accordingly, respiration measurements during seed dehydration demonstrated that intermediate seeds with the highest DT levels are better prepared to cease respiration and avoid oxidative stresses.

2020-05-26 | PXD015806 | Pride

Project description:WT1 vs DT mouse

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Acinetobacter baumannii strain:DT-544 | isolate:DT-544

Project description:Acinetobacter baumannii strain:DT-544 | isolate:DT-544 Genome sequencing and assembly

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ChIP-seq profile of RPA in B upon HU treatment

Project description:In this study, we map sites of replication initiation and breakage in primary cells at high resolution under conditions of replication stress. We show that replication initiates between transcribed genes within nucleosome-depleted structures established by long asymmetrical poly(dA:dT) tracts flanking the initiation site. Paradoxically, large (>20 bp) homopolymeric (dA/dT) tracts are also preferential sites of polar replication fork stalling and collapse. We propose that the evolutionary expansion of poly(dA:dT) tracts in eukaryotic genomes serves to promote replication initiation, but at the cost of increasing chromosome fragility.

2018-08-01 | GSE116320 | GEO

Project description:Species description of DT strains

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Edwardsiella tarda DT strain:DT

Project description:Edwardsiella tarda DT genome sequencing

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Molecular dissection of drought tolerance mechanisms in rice by comparative deep transcriptome sequencing

Project description:To dissect the molecular mechanisms underlying drought tolerance (DT) in rice, transcriptome differences of a DT introgression line H471, the DT donor P28 and the drought sensitive recurrent parent HHZ under drought stress were investigated using deep transcriptome sequencing. Results revealed a differential constitutive gene expression prior to stress and distinct global transcriptome reprogramming among three genotypes under time-series drought stress, consistent with their differential genotypes and DT phenotypes.

2014-12-30 | GSE57950 | GEO

Cell killing by iHAP and DT-061 is not through PP2A-B56 activation

Project description:PP2A is an abundant ser/thr protein phosphatase that act as a tumor suppressor by antagonizing multiple oncogenic kinases. For this reason, compounds able to activate PP2A holoenzymes are attractive anticancer agents. DT-061 and iHAP are phenothiazine derivatives that have recently been claimed to activate specific PP2A-B56 complexes to mediate cell killing. Here we show that iHAP and DT-061 do not activate PP2A-B56 complexes in vitro and that CRISPR removal of B56 regulatory subunits does not affect cellular toxicity of the compounds. Through genome-wide CRISPR screens we uncover the cell killing mechanism of iHAP and DT-061. We find that iHAP is a microtubule poison and removal of mitotic regulators causes hypersensitivity. In contrast, DT-061 disrupts both Golgi and ER consistent with an impact on cellular lipid composition. Indeed, we directly visualize DT-061 in cytoplasmic granules that co-localize with Golgi markers shortly after addition of the compound. Our work uncovers that well known side-effects of phenothiazine derived compounds cause cell killing by iHAP and DT-061 arguing that these compounds cannot be used for dissecting PP2A biology.

2021-06-11 | MSV000087616 | MassIVE

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