Aquatic metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA261440 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Biodegradation of organic micropollutants in GAC filters – temporal development and spatial variations
| PRJEB71093 | ENA
Project description:The SAR11 clade is one of the most abundant bacterioplankton groups in surface waters of most of the oceans and lakes. However, only 15 SAR11 phages have been isolated thus far, and only one of them belongs to the Myoviridae family (pelagimyophages). Here, we have analyzed 26 sequences of myophages that putatively infect the SAR11 clade. They have been retrieved by mining ca. 45 Gbp aquatic assembled cellular metagenomes and viromes. Most of the myophages were obtained from the cellular fraction (0.2 μm), indicating a bias against this type of virus in viromes. We have found the first myophages that putatively infect Candidatus Fonsibacter (freshwater SAR11) and another group putatively infecting bathypelagic SAR11 phylogroup Ic. The genomes have similar sizes and maintain overall synteny in spite of low average nucleotide identity values, revealing high similarity to marine cyanomyophages. Pelagimyophages recruited metagenomic reads widely from several locations but always much more from cellular metagenomes than from viromes, opposite to what happens with pelagipodophages. Comparing the genomes resulted in the identification of a hypervariable island that is related to host recognition. Interestingly, some genes in these islands could be related to host cell wall synthesis and coinfection avoidance. A cluster of curli-related proteins was widespread among the genomes, although its function is unclear.IMPORTANCE SAR11 clade members are among the most abundant bacteria on Earth. Their study is complicated by their great diversity and difficulties in being grown and manipulated in the laboratory. On the other hand, and due to their extraordinary abundance, metagenomic data sets provide enormous richness of information about these microbes. Given the major role played by phages in the lifestyle and evolution of prokaryotic cells, the contribution of several new bacteriophage genomes preying on this clade opens windows into the infection strategies and life cycle of its viruses. Such strategies could provide models of attack of large-genome phages preying on streamlined aquatic microbes.
| S-EPMC7029224 | biostudies-literature
Project description:We identified several hub genes and key pathways associated with GAC initiation and progression by analysising the microarray data on DEGs, whcih provided a detailed molecular mechanism underlying GAC occurrence and progression.
2019-06-10 | GSE118916 | GEO
Project description:Dysregulated transcription due to disruption in histone lysine methylation dynamics is an established contributor to tumorigenesis. However, whether analogous pathologic epigenetic mechanisms act directly on the ribosome to advance oncogenesis is unclear. Here we find that trimethylation of the core ribosomal protein L40 at lysine 22 (rpL40K22me3) by the lysine methyltransferase (KMT) SMYD5 regulates mRNA translation output to promote gastric adenocarcinoma (GAC) malignant progression with lethal peritoneal ascites. A biochemical-proteomic strategy identifies the mono-ubiquitin fusion protein partner rpL40 as the principal physiologic substrate of SMYD5 across diverse samples. Inhibiting the SMYD5-rpL40K22me3 axis in GAC cell lines reprograms protein synthesis to attenuate oncogenic gene expression signatures. SMYD5 and rpL40K22me3 are upregulated in GAC patient samples and negatively correlate with clinical outcomes. SMYD5 ablation in vivo in familial and sporadic mouse models of malignant GAC blocks metastatic disease including peritoneal carcinomatosis (PC). Suppressing SMYD5 methylation of rpL40 inhibits human cancer cell and patient-derived GAC xenograft growth and renders them hypersensitive to PI3K/mTOR inhibitors. Finally, combining SMYD5 depletion with PI3K/mTOR inhibition and CAR-T administration cures an otherwise lethal in vivo mouse model of aggressive GAC-derived PC. Together, our work uncovers a ribosome-based epigenetic mechanism that facilitates evolution of malignant GAC and nominates SMYD5 targeting as part of a potential cornerstone combination therapy to treat a deadly cancer.
2024-03-01 | GSE238257 | GEO
Project description:The gene GLS generates the phosphate activated glutaminase C (GAC) isoform by alternative splicing. GAC, compared to the other isoform, kidney-type glutaminase (KGA), has been characterized as more active and particularly important for cancer cell growth. Very little is known about post-translational modifications regulating GAC function. Hereby we describe the identification of a phosphorylation on the serine 95, located at the GLS N-terminus, a domain shared by both isoforms. A GAC phosphomimetic mutant (S95D) ectopically expressed in breast cancer cells presented decreased enzymatic activity, and its expression impacted on cell’s glutamine uptake, glutamate release and intracellular glutamate levels (compared to expressing wild type GAC) without changing GAC sub-cellular localization. Curiously, replacing S95 by an alanine in the ectopically expressed GAC (S95A) increased cell proliferation and migration. Taken together, these results reveal that GAC is post-translationally regulated by phosphorylation, which impacts on cancer phenotype.
2018-08-13 | PXD008338 | Pride
Project description:We developed an extraction-free qPCR assay to identify Omicron BA.1 cases and verified lineage by sequencing. We find that BA.2 variants show almost twice the viral load (Ct) compared to both BA.1 as well as Delta variants.
2022-05-25 | E-MTAB-11650 | biostudies-arrayexpress
Project description:Sand filters Targeted loci environmental
| PRJNA304222 | ENA