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Induction of a transcriptional adaptation response via perturbations at the DNA and RNA levels

ABSTRACT: Induction of a transcriptional adaptation response via perturbations at the DNA and RNA levels

PROVIDER: PRJNA1073549 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27878174_1.fastq.gz	Fastqsanger.gz
	SRR27878174_2.fastq.gz	Fastqsanger.gz
	SRR27878175_1.fastq.gz	Fastqsanger.gz
	SRR27878175_2.fastq.gz	Fastqsanger.gz
	SRR27878176_1.fastq.gz	Fastqsanger.gz

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Induction of a transcriptional adaptation response via perturbations at the DNA and RNA levels [dst233]

Project description:Induction of a transcriptional adaptation response via perturbations at the DNA and RNA levels [dst233]

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Induction of a transcriptional adaptation response via perturbations at the DNA and RNA levels [dst233]

Project description:Transcriptional adaptation (TA) is a cellular process whereby mRNA-destabilizing mutations lead to the transcriptional upregulation of so-called adapting genes. The nature of the TA-triggering factor(s) remains unclear. Here, we first generated Cas9-induced mutations in mouse Actg1, including an mRNA-destabilizing allele and an RNA-less allele. We find in the Actg1 mRNA-destabilizing allele, higher levels of Actg2 mRNA as well as increased chromatin accessibility at the Actg2 locus compared with wild-type and the RNA-less allele. Notably, Cas13d experiments show that Actg1 mRNA cleavage, but not Actg1 pre-mRNA cleavage, also triggers Actg2 upregulation; however, this upregulation is not associated with increased chromatin accessibility at the Actg2 locus. Furthermore, time course experiments show that increased Actg2 expression persists even after Actg1 mRNA degradation by Cas13d ceases. Together, our data highlight the importance of cytoplasmic mRNA degradation as a trigger for the TA response and suggest that chromatin remodeling is not necessary for TA.

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Induction of a transcriptional adaptation response via perturbations at the DNA and RNA levels

Project description:This SuperSeries is composed of the SubSeries listed below.

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Phosphorylation controls mRNA retention via nuclear speckle cohesion during environmental perturbations

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Induction of a transcriptional adaptation response by RNA destabilization events [dst278]

Project description:Transcriptional adaptation (TA) is a cellular process whereby mRNA-destabilizing mutations lead to the transcriptional upregulation of so-called adapting genes. The nature of the TA-triggering factor(s) remains unclear, namely whether an mRNA-borne premature termination codon (PTC) or the subsequent mRNA degradation process, and/or its products, elicits TA. Here, we first established two perturbations leading to mRNA destabilization for mouse Actg1: a Cas9-induced mutation that leads to a PTC, and Cas13d-mediated mRNA cleavage. We find that both perturbations are effective in degrading Actg1 mRNA and upregulating Actg2. Notably, increased chromatin accessibility at the Actg2 locus was observed only in the Cas9-induced mutant allele but not in the Cas13d-targeted cells, suggesting that chromatin remodeling is not required for Actg2 upregulation. We further show that ribozyme-mediated Actg1 pre-mRNA cleavage also leads to a robust upregulation of Actg2. Together, these data highlight the critical role of RNA destabilization events as a trigger for TA.

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Induction of a transcriptional adaptation response by RNA destabilization events [dst175]

Project description:Induction of a transcriptional adaptation response by RNA destabilization events [dst175]

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Induction of a transcriptional adaptation response by RNA destabilization events [dst278]

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Deciphering the transcriptional adaptation of Corynebacterium glutamicum in transition from aerobiosis via microaerobiosis to anaerobiosis via RNA-seq

Project description:To investigate the adaptation of Corynebacterium glutamicum to altering oxygen availabilities, we conceived a triple-phase fermentation process that describes a gradual reduction of dissolved oxygen depicting a shift from aerobiosis via microaerobiosis to anaerobiosis. The distinct process phases were clearly bordered by the bacteria’s physiologic response such as reduced growth rate, biomass substrate yield and altered yield of fermentation products. During the process, sequential samples were drawn at six points and analyzed via RNA-sequencing of Illumina TruSeq Stranded mRNA libaries sequenced paired end on an Illumina MiSeq system using 75 nt read length. We found transcriptional alterations of almost 50 % (1421 genes) of the entire protein coding genes and observed an upregulation of fermentative pathways, a rearrangement of respiration and mitigation of the basic cellular mechanisms such as transcription, translation and replication as a transient response related to the installed oxygen dependent process phases.

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Potent and uniform fetal hemoglobin induction via base editing

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Mycobacterium tuberculosis Lsr2 is a global transcriptional regulator required for adaptation to changing oxygen levels and virulence

Project description:To survive a dynamic host environment, Mycobacterium tuberculosis must endure a series of challenges from reactive oxygen and nitrogen stress, to drastic shifts in oxygen availability. The mycobacterial Lsr2 protein has been implicated in reactive oxygen defense via direct protection of DNA. To examine the role of Lsr2 in pathogenesis and physiology of M. tuberculosis, we generated a strain deleted for lsr2. Analysis of the M. tuberculosis ?lsr2 strain demonstrated that Lsr2 is not required for DNA protection, as this strain was as equally susceptible as the wild-type to DNA-damaging agents. The lsr2 mutant did display severe growth defects under normoxic and hyperoxic conditions, but was not required for growth under low oxygen conditions. However, it was also required for adaptation to anaerobiosis. The defect in anaerobic adaptation led to a marked decrease in viability during, as well as a lag in recovery from, anaerobiosis. Gene expression profiling of ?lsr2 under aerobic and anaerobic conditions in conjunction with published DNA binding-site data indicate that Lsr2 is a global transcriptional regulator controlling adaptation to changing oxygen levels. The ?lsr2 strain was capable of establishing an early infection in the Balb/c mouse model; however, it was severely defective in persisting in the lungs and caused no discernible lung pathology. These findings demonstrate M. tuberculosis Lsr2 is a global transcriptional regulator required for control of genes involved in adaptation to extremes in oxygen availability and is required for persistent infection. Wild type H37Rv or lsr2 mutant strains were grown aerobically or in a Rach dormancy model in dubos tween albumin media and analyzed. Alternately, either aerobically grown or Rach model hypoxic samples were challenged with H2O2 samples and harvested 1h later. Experiments were repeated in triplicate or quadruplicate.

2014-05-24 | E-GEOD-57948 | biostudies-arrayexpress

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