Arid soil microbiome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA729590 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15047000_1.fastq.gz | Fastqsanger.gz | |||
| SRR15047000_2.fastq.gz | Fastqsanger.gz | |||
| SRR15047100_1.fastq.gz | Fastqsanger.gz | |||
| SRR15047100_2.fastq.gz | Fastqsanger.gz | |||
| SRR15047001_1.fastq.gz | Fastqsanger.gz |
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Project description:Every known SWI/SNF chromatin-remodeling complex incorporates an ARID DNA binding domain-containing subunit. Despite being a ubiquitous component of these complexes, physiological roles for this domain remain undefined. We screened an N-ethyl-N-nitrosurea (ENU) mutagenized library for ARID domain point mutations and generated an Arid1a/Baf250a hypomorphic allele. The mutant ARID1a (V1068G) protein is stably expressed at wild-type levels, and it is capable of assembling into a SWI/SNF complex with in vitro mononucleosome disruption activity. However, its capacity to bind DNA is lost. Consistent with defective DNA binding, mutant protein occupancy at known SWI/SNF target genes is decreased. Loss of DNA binding is associated with concurrent changes in SWI/SNF target gene expression. Mutant embryos manifest heart defects, fail to establish proper yolk sac vasculature, and exhibit hemorrhaging. As a result of these phenotypes, mutant embryos fail to establish proper circulation, culminating in ischemic arrest in utero between days 9.5 and 11.5. These data support a role for ARID1a-containing, BAF-A complexes in heart and extraembryonic vascular development, and indicate the ARID domain of ARID1a is essential in this regard. Hence, intrinsic ARID subunit-DNA interactions are required for normal SWI/SNF function in vivo. Four-condition experiment, wild-type vs Baf250a/Arid1a^V1068G/V1068G yolk sacs isolated at E8.5 and E9.5. Biological replicates: 3 per condition.
2012-01-15 | E-GEOD-32116 | biostudies-arrayexpress
Project description:Every known SWI/SNF chromatin-remodeling complex incorporates an ARID DNA binding domain-containing subunit. Despite being a ubiquitous component of the complex, physiological roles for this domain remain undefined. Here we show that disruption of ARID1a-DNA binding in mice results in embryonic lethality, with mutant embryos manifesting prominent defects in the heart and extraembryonic vasculature. The DNA binding defective mutant ARID1a subunit is stably expressed and capable of assembling into a SWI/SNF complex with chromatin remodeling activity, but promoter occupancy by ARID1a-containing, SWI/SNF complexes (BAF-A) is impaired. Depletion of ARID domain-dependent, BAF-A associations at THROMBOSPONDIN 1 (THBS1) led to the concomitant upregulation of this anti-angiogenic protein. Using a THBS1 promoter-reporter gene, we further show that BAF-A directly regulates THBS1 promoter activity in an ARID domain-dependent manner. Our data not only demonstrate that ARID-DNA interactions are physiologically relevant in higher eukaryotes, but also indicate these interactions can facilitate SWI/SNF binding to target sites in vivo. These findings support the model wherein cooperative interactions among intrinsic subunit-chromatin interaction domains and sequence-specific transcription factors drive SWI/SNF recruitment.
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Project description:ARID (AT-rich interacting domain) proteins are a heterogeneous family of DNA-binding proteins involved in transcriptional regulation. No precise DNA-binding preferences have yet been defined for the aberrant member Arid5a. In addition, the protein binds to mRNA motifs for transcript stabilisation, presumably through the DNA-binding ARID domain. Here we first provide an unbiased definition of RNA motifs and a clear breakdown of nucleic acid binding by the ARID domain. An RNA Bind-n-Seq (RBNS) experiment was performed to find a consensus motif of the Arid5a domain. It reveals a preference for an unexpected CAGGCAG consensus motif, accompanied by a general preference for AU-rich motifs.
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Project description:Higher aridity and more extreme rainfall events in drylands are predicted under climate change. Yet it is unclear how changing precipitation regimes may affect nitrogen (N) cycling, especially in areas with extremely high aridity. Here we investigated soil N isotopic values (M-NM-415N) along a 3200 km aridity gradient and show a hump-shaped relationship between soil M-NM-415N and aridity index (AI) with a threshold at AI=0.32. Also, using a micro-array metageomics tool named GeoChip 5.0, we showed that Variations of nitrification and denitrification gene abundance along the gradient which provide further evidence for the existence of this threshold. Data support the hypothesis that the increase of gaseous N losses is higher than the increase of net plant N accumulation with increasing AI below AI=0.32, while the opposite is favoured above this threshold. Our results suggest the importance of N-cycling microbes in extremely dry areas and the different controlling factors of N cycling on the either side of the threshold.
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