Search results for "Repressor lexA"

showing 4 items of 4 documents

Establishment of Polycomb silencing requires a transient interaction between PC and ESC

2001

Two distinct types of Polycomb complexes have been identified in flies and in vertebrates, one containing ESC and one containing PC. Using LexA fusions, we show that PC and ESC can establish silencing of a reporter gene but that each requires the presence of the other. In early embryonic extracts, we find PC transiently associated with ESC in a complex that includes EZ, PHO, PH, GAGA, and RPD3 but not PSC. In older embryos, PC is found in a complex including PH, PSC, GAGA, and RPD3, whereas ESC is in a separate complex including EZ, PHO, and RPD3.

Polycomb-Group ProteinsRepressorSettore BIO/11 - Biologia MolecolarePlasma protein bindingBiologyPolycomb silencingResearch CommunicationGeneticsPolycomb-group proteinsAnimalsDrosophila ProteinsGene silencingGene Silencingreproductive and urinary physiologyPolycomb Repressive Complex 1Reporter geneurogenital systemPolycomb Repressive Complex 2PcG complexEmbryoHistone-Lysine N-MethyltransferasePrecipitin TestsEmbryonic stem cellMolecular biologyRepressor Proteinsembryonic structuresInsect ProteinsDrosophilaRepressor lexAbiological phenomena cell phenomena and immunityESC/PHOProtein BindingDevelopmental BiologyGenes & Development
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The Use and Abuse of LexA by Mobile Genetic Elements

2016

The SOS response is an essential process for responding to DNA damage in bacteria. The expression of SOS genes is under the control of LexA, a global transcription factor that undergoes self-cleavage during stress to allow the expression of DNA repair functions and delay cell division until the damage is rectified. LexA also regulates genes that are not part of this cell rescue program, and the induction of bacteriophages, the movement of pathogenicity islands, and the expression of virulence factors and bacteriocins are all controlled by this important transcription factor. Recently it has emerged that when regulating the expression of genes from mobile genetic elements (MGEs), LexA often …

0301 basic medicineMicrobiology (medical)Transcription GeneticDNA repair030106 microbiologyRegulatorBiologyRegulonMicrobiology03 medical and health sciencesBacterial ProteinsVirologyGene expressionBacteriophagesSOS responseSOS Response GeneticsTranscription factorGeneGeneticsSerine Endopeptidasesbiochemical phenomena metabolism and nutritionInterspersed Repetitive Sequencesenzymes and coenzymes (carbohydrates)Infectious DiseasesbacteriaRepressor lexACorepressorDNA DamageTrends in Microbiology
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Phage-borne factors and host LexA regulate the lytic switch in phage GIL01.

2011

ABSTRACT The Bacillus thuringiensis temperate phage GIL01 does not integrate into the host chromosome but exists stably as an independent linear replicon within the cell. Similar to that of the lambdoid prophages, the lytic cycle of GIL01 is induced as part of the cellular SOS response to DNA damage. However, no CI-like maintenance repressor has been detected in the phage genome, suggesting that GIL01 uses a novel mechanism to maintain lysogeny. To gain insights into the GIL01 regulatory circuit, we isolated and characterized a set of 17 clear plaque ( cp ) mutants that are unable to lysogenize. Two phage-encoded proteins, gp1 and gp7, are required for stable lysogen formation. Analysis of …

Gene Expression Regulation ViralvirusesBacteriophages Transposons and PlasmidsBacillus thuringiensisBacillus PhagesBiologyMicrobiologyHost-Parasite InteractionsBacteriolysisLysogenBacterial ProteinsLysogenic cycleHost chromosomeSOS responseSOS Response GeneticsMolecular BiologyLysogenyGeneticsBinding SitesSerine Endopeptidasesbiochemical phenomena metabolism and nutritionBacillus PhageTemperatenessLytic cycleDNA ViralbacteriaVirus ActivationRepressor lexAProtein BindingJournal of bacteriology
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Bacteriophage GIL01 gp7 interacts with host LexA repressor to enhance DNA binding and inhibit RecA-mediated auto-cleavage

2015

The SOS response in Eubacteria is a global response to DNA damage and its activation is increasingly associated with the movement of mobile genetic elements. The temperate phage GIL01 is induced into lytic growth using the host's SOS response to genomic stress. LexA, the SOS transcription factor, represses bacteriophage transcription by binding to a set of SOS boxes in the lysogenic promoter P1. However, LexA is unable to efficiently repress GIL01 transcription unless the small phage-encoded protein gp7 is also present. We found that gp7 forms a stable complex with LexA that enhances LexA binding to phage and cellular SOS sites and interferes with RecA-mediated auto-cleavage of LexA, the ke…

Gene Expression Regulation ViralSOS responsebacteriophagesTranscription GeneticvirusesRepressorBacillus PhagesBiologybakteriofagitBacteriophage03 medical and health sciencesSOS Response (Genetics)Viral ProteinsBacterial ProteinsLysogenic cycleGeneticsSOS responsePromoter Regions GeneticSOS Response GeneticsTranscription factor030304 developmental biologyGenetics0303 health sciences030306 microbiologyLexA repressorGene regulation Chromatin and EpigeneticsSerine Endopeptidasesta1182DNAbiochemical phenomena metabolism and nutritionbiology.organism_classification3. Good healthCell biologyRepressor Proteinsenzymes and coenzymes (carbohydrates)Rec A RecombinasesLytic cyclebacteriaRepressor lexAProtein BindingNucleic Acids Research
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