Arthrobacter silvisoli strain:NEAU-SA1
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ABSTRACT:
PROVIDER: PRJNA483384 | ENA |
REPOSITORIES: ENA
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Project description:Arthrobacter chlorophenolicus A6 is a 4-chlorophenol degrading soil bacterium with high phyllosphere colonization capacity. Till now the genetic basis for the phyllosphere competency of Arthrobacter or other pollutant-degrading bacteria is uncertain. We investigated global gene expression profile of A. chlorophenolicus grown in the phyllosphere of common bean (Phaseolus vulgaris) compared to growth on agar surfaces.
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Project description:Arthrobacter chlorophenolicus A6 is a 4-chlorophenol degrading soil bacterium with high phyllosphere colonization capacity. Till now the genetic basis for the phyllosphere competency of Arthrobacter or other pollutant-degrading bacteria is uncertain. We investigated global gene expression profile of A. chlorophenolicus grown in the phyllosphere of common bean (Phaseolus vulgaris) compared to growth on agar surfaces. We designed transcriptome arrays and investigated which genes had different transcript levels in the phyllosphere of common bean (Phaseolus vulgaris) as compared to agar surfaces. Since water availability is considered an important factor in phyllosphere survival and activity, we included both high and low relative humidity treatments for the phyllosphere-grown cells. In addition, we determined the expression profile under pollutant exposure by the inclusion of two agar surface treatments, i.e. with and without 4-chlorophenol.
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Project description:Vertebrates have two cohesin complexes that consist of Smc1, Smc3, Rad21/Scc1 and either SA1 or SA2, but their functional specificity is unclear. Mouse embryos lacking SA1 show developmental delay and die before birth. Comparison of the genome wide distribution of cohesin in wild-type and SA1-null cells reveals that SA1 is largely responsible for cohesin accumulation at promoters and at sites bound by the insulator protein CTCF. As a consequence, ablation of SA1 alters transcription of genes involved in biological processes related to Cornelia de Lange syndrome (CdLS), a genetic disorder linked to dysfunction of cohesin. We show that the presence of cohesin-SA1 at the promoter of myc and of protocadherin genes positively regulates their expression, a task that cannot be assumed by cohesin-SA2. Cohesin binding pattern along some gene clusters is also affected by the lack of SA1, leading to dysregulation of the genes within. We hypothesize that impaired cohesin-SA1 function in gene expression underlies the molecular etiology of CdLS. Two-condition experiment, SA1 KO vs. WT cells. 3 Biological replicates.
2012-03-15 | E-GEOD-32234 | biostudies-arrayexpress
Project description:Vertebrates have two cohesin complexes that consist of Smc1, Smc3, Rad21/Scc1 and either SA1 or SA2, but their functional specificity is unclear. Mouse embryos lacking SA1 show developmental delay and die before birth. Comparison of the genome wide distribution of cohesin in wild-type and SA1-null cells reveals that SA1 is largely responsible for cohesin accumulation at promoters and at sites bound by the insulator protein CTCF. As a consequence, ablation of SA1 alters transcription of genes involved in biological processes related to Cornelia de Lange syndrome (CdLS), a genetic disorder linked to dysfunction of cohesin. We show that the presence of cohesin-SA1 at the promoter of myc and of protocadherin genes positively regulates their expression, a task that cannot be assumed by cohesin-SA2. Cohesin binding pattern along some gene clusters is also affected by the lack of SA1, leading to dysregulation of the genes within. We hypothesize that impaired cohesin-SA1 function in gene expression underlies the molecular etiology of CdLS.
2012-03-15 | GSE32234 | GEO
Project description:Vertebrates have two cohesin complexes that consist of Smc1, Smc3, Rad21/Scc1 and either SA1 or SA2, but their functional specificity is unclear. Mouse embryos lacking SA1 show developmental delay and die before birth. Comparison of the genome wide distribution of cohesin in wild-type and SA1-null cells reveals that SA1 is largely responsible for cohesin accumulation at promoters and at sites bound by the insulator protein CTCF. As a consequence, ablation of SA1 alters transcription of genes involved in biological processes related to Cornelia de Lange syndrome (CdLS), a genetic disorder linked to dysfunction of cohesin. We show that the presence of cohesin-SA1 at the promoter of myc and of protocadherin genes positively regulates their expression, a task that cannot be assumed by cohesin-SA2. Cohesin binding pattern along some gene clusters is also affected by the lack of SA1, leading to dysregulation of the genes within. We hypothesize that impaired cohesin-SA1 function in gene expression underlies the molecular etiology of CdLS. Examination of genome wide distribution of cohesin subunits in wildtype and SA1-null cells
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