Methyloligella sp. GL2
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA637368 | ENA |
REPOSITORIES: ENA
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Project description:Targeted therapies against cancer stem cells which are enriched in side populations (SP) involves interruption of Wnt-signalling. Furthermore, EpCAM is a SP marker and modulator of Wnt-signalling. Therefore, the effects of an anti-EpCAM treatment on SP-cells and WNT/β-catenin signalling was studied. SP of the human lung adenocarcinoma cell line A549 was obtained by fluorescence activated cell sorting and whole genome scans helped to define their molecular phenotype after anti-EpCAM antibody treatment.
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Project description:Targeted therapies against cancer stem cells which are enriched in side populations (SP) involves interruption of Wnt-signalling. Furthermore, EpCAM is a SP marker and modulator of Wnt-signalling. Therefore, the effects of an anti-EpCAM treatment on SP-cells and WNT/β-catenin signalling was studied. SP of the murine lung adenocarcinoma cell line A2C12 was obtained by fluorescence activated cell sorting and whole genome scans helped to define their molecular phenotype after anti-EpCAM antibody treatment.
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Project description:In previous work in our group, shotgun genome sequencing of Arthrobacter sp. revealed potential new P450 monooxygenases and many other oxidoreductases with putative hydroxylation activity. A targeted approach to identify enzymes involved in the degradation of certain molecules is proteomic analysis. In the case of growth on certain substances, enzymes like P450s, which are responsible for the observed organism’s capabilities, might be overexpressed or initially induced.
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Project description:Macrophages play fundamental roles in regulation of inflammatory responses to pathogens, resolution of inflammation and tissue repair, and maintenance of tissue homeostasis. The long (L) and short (S) isoforms of SP-R210/MYO18A, a macrophage receptor for surfactant protein A (SP-A) and C1q, regulate basal and inflammatory macrophage phenotype at multiple gene expression, translational, and subcellular levels in addition to their SP-A and C1q-mediated functions; disruption of L renders macrophages hyper-inflammatory, although the underlying mechanism had previously been unexplored. We questioned whether disruption of the L isoform would alter the global genomic responses. RNA sequencing analysis of SP-R210L(DN) macrophages revealed basal and influenza induced upregulation of genes associated with inflammatory pathways, including TLR, RIG-I, NOD, and cytoplasmic DNA signaling, whereas knockdown of both SP-R210 isoforms (L and S) only resulted in increased RIG-I and NOD signaling. Chromatin immunoprecipitation sequencing (ChIP-seq) analysis showed increased genome-wide deposition of the pioneer transcription factor PU.1 in SP-R210L(DN) compared to WT cells. ChIP-seq analysis of histone H3 methylation showed alterations in both repressive (H3K9me3 and H3K27me3) and transcriptionally active (H3K9me3) histone marks. Influenza A virus (IAV) infection, which stimulates an array of cytosolic and TLR-mediated antiviral mechanisms, resulted in differential redistribution between proximal promoter and distal sites and decoupling of PU.1 binding from Toll-like receptor regulated gene promoters in SP-R210L(DN) cells. Our findings suggest that SP-R210L-deficient macrophages are poised with an open PU.1-primed chromatin conformation to rapidly respond to inflammatory and metabolic stimuli.
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Project description:GLABRA2 (GL2) is a class IV homeodomain leucine-zipper (HD-Zip IV) transcription factor that is critical for the differentiation of the epidermis in the plant model Arabidopsis. HD-Zip IV transcription factors are characterized by the presence of a lipid sensing domain known as START (for STeroidogenic Acute Regulatory (StAR)-related lipid Transfer). Genome-wide ChIP-seq assays were performed with seedlings expressing EYFP-tagged GL2 wild-type and mutant proteins to test whether the START domain is dispensible for DNA binding in vivo. These experiments included three START domain mutants (gl2_∆ST (listed here as gl2_dSTART), gl2_Amo, and gl2_E375G;R392M) as well as a mutant deleted for the six terminal amino acids of the HD and the entire leucine zipper (gl2_∆HD6;∆ZLZ (listed here as gl2_dZip)). Data analysis revealed DNA binding proficiency for wild-type GL2 and for all three START domain mutants whereas little or no binding was detected for gl2∆HD6;∆ZLZ and the gl2-5 null mutant control. Genomic distributions of the binding sites were similar for wild-type GL2 and the START domain mutants. Most of the ChIP-seq hits were mapped to promoter or intergenic regions, consistent with the role of GL2 as a transcriptional regulator. The relative positions of the binding sites to the transcription start sites were also similar. Gene ontology (GO) classification revealed overlapping functional classes of target genes bound by wild-type GL2 and the START domain mutants.
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