Zambian_milk_HCMV
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB31143 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR3163180_1.fastq.gz | Fastqsanger.gz | |||
| ERR3163180_2.fastq.gz | Fastqsanger.gz | |||
| ERR3163330_1.fastq.gz | Fastqsanger.gz | |||
| ERR3163330_2.fastq.gz | Fastqsanger.gz | |||
| ERR3163181_1.fastq.gz | Fastqsanger.gz |
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Project description:High-temperature stress (HTS) is one of the main environmental stresses that limit plant growth and crop production in agricultural systems. Maca (Lepidium meyenii) is an important high-altitude herbaceous plant adapted to a wide range of environmental stimuli such as cold, strong wind and UV-B exposure. However, it is an extremely HTS-sensitive plant species. Thus far, there is limited information about gene/protein regulation and signaling pathways related to the heat stress responses in maca. In this study, proteome profiles of maca seedlings exposed to HTS for 12 h were investigated using a tandem mass tag (TMT)-based proteomic approach. In total, 6,966 proteins were identified, of which 300 showed significant alterations in expression following HTS. Bioinformatics analyses indicated that protein processing in endoplasmic reticulum was the most significantly up-regulated metabolic pathway following HTS. Quantitative RT-PCR (qRT-PCR) analysis showed that the expression levels of 19 genes encoding proteins mapped to this pathway were significantly up-regulated under HTS. These results show that protein processing in the endoplasmic reticulum may play a crucial role in the responses of maca to HTS. Our proteomic data can be a good resource for functional proteomics of maca and our results may provide useful insights into the molecular response mechanisms underlying herbal plants to HTS.
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Project description:High-throughput sequencing (HTS) has become a powerful tool for the detection of and sequence characterization of microRNAs (miRNA) and other small RNAs (sRNA). Unfortunately, the use of HTS data to determine the relative quantity of different miRNAs in a sample has been shown to be inconsistent with quantitative PCR and Northern Blot results. Several recent studies have concluded that the major contributor to this inconsistency is bias introduced during the construction of sRNA libraries for HTS and that the bias is primarily derived from the adaptor ligation steps; specifically where single stranded adaptors are sequentially ligated to the 3' and 5'-end of sRNAs using T4 RNA ligases. In this study we investigated the effects of ligation bias by using a pool of randomized ligation substrates, defined mixtures of miRNA sequences and several combinations of adaptors in HTS library construction. We show that like the 3' adaptor ligation step, the 5' adaptor ligation is also biased, not because of primary sequence, but instead due to secondary structures of the two ligation substrates. We find that multiple secondary structural factors influence final representation in HTS results. Our results provide insight about the nature of ligation bias and allowed us to design adaptors that reduce ligation bias and produce HTS results that more accurately reflect the actual concentrations of miRNAs in the defined starting material.
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Project description:Human Cytomegalovirus (HCMV) causes severe morbidity and mortality in an immune-compromised or immune-naïve host. Among DNA viruses, the genetic diversity of HCMV is unexpectedly high and comparable to those of RNA viruses, which hinders the development of effective vaccines and causes the emergence of antiviral resistance. However, little is known about how HCMV acquires genetic variation. Here, we propose an evolution strategy of HCMV, that exploits host “jumping DNA” L1 retrotransposon as a mutagen. We found that HCMV infection switches on L1 expression by upregulating transcription factors YY1 and RUNX3. Furthermore, HCMV DNA processivity factor, UL44 recruits L1 ribonucleoproteins to viral replication compartments and induces DNA damage to its genome. Deep-sequencing analysis of cultured HCMV genome revealed that L1 retrotransposon facilitates mutation burden on the viral genome. Indeed, laboratory adaptation of HCMV to fibroblasts is only observed upon active L1 expression. These findings demonstrate the evolution mechanism and molecular insights of how HCMV acquires genetic fitness by the hijacking of host L1 retrotransposon.
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Project description:Human cytomegalovirus (HCMV) infects up to 80% of the world’s population and is linked to serious morbidity in immunocompromised individuals and newborns. Here, using multiple genome-scale assays and computational approaches, we show that HCMV infection leads to widespread changes in chromatin accessibility and chromatin looping, with hundreds of thousands of human genomic regions affected 48 hours after infection. Integrative analyses reveal that HCMV infection perturbs the Hippo signaling pathway by drastically diminishing TEA domain transcription factor 1 (TEAD1) activity. Chromatin immunoprecipitation experiments confirm extensive concordant loss of TEAD1 binding and H3K27ac active histone marks upon infection. TEAD transcription factors are direct effectors of the Hippo signaling pathway, and our data support a position for TEAD1 at the top of a hierarchy involving key developmental pathways with differential expression subsequent to HMCV infection. Known gene targets of TEAD1, including Cellular Communication Network Factor 1 (CCN1) and Thrombospondin 1 (THBS1), are significantly downregulated with HCMV infection, reflecting diminished TEAD1-mediated activity. HCMV infection reduces TEAD1 binding through four distinct mechanisms: closing of TEAD1-bound chromatin, reduction of Yes1 associated transcriptional regulator (YAP1) and phosphorylated YAP (pYAP1) levels, reduction of TEAD1 transcript and protein levels, and alteration of TEAD1 exon-6 usage. Collectively, these comprehensive genome-scale analyses reveal novel mechanisms induced by HCMV infection.
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