Multiple genes recruited from hormone pathways partition maize diterpenoid defences.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA491716 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Duplication and divergence of primary pathway genes underlie the evolution of plant specialized metabolism; however, mechanisms partitioning parallel hormone and defence pathways are often speculative. For example, the primary pathway intermediate ent-kaurene is essential for gibberellin biosynthesis and is also a proposed precursor for maize antibiotics. By integrating transcriptional coregulation patterns, genome-wide association studies, combinatorial enzyme assays, proteomics and targeted mutant analyses, we show that maize kauralexin biosynthesis proceeds via the positional isomer ent-isokaurene formed by a diterpene synthase pair recruited from gibberellin metabolism. The oxygenation and subsequent desaturation of ent-isokaurene by three promiscuous cytochrome P450s and a new steroid 5α reductase indirectly yields predominant ent-kaurene-associated antibiotics required for Fusarium stalk rot resistance. The divergence and differential expression of pathway branches derived from multiple duplicated hormone-metabolic genes minimizes dysregulation of primary metabolism via the circuitous biosynthesis of ent-kaurene-related antibiotics without the production of growth hormone precursors during defence.
2019-07-01 | GSE120135 | GEO
Project description:Multiple genes recruited from hormone pathways partition maize diterpenoid defences.
2020-04-06 | E-GEOD-120135 | ExpressionAtlas
Project description:Host innate immune defences play a critical role in restricting the intracellular propagation and pathogenesis of invading viral pathogens. Here we show that the histone H3.3 chaperone HIRA (histone cell cycle regulator) associates with promyelocytic leukaemia nuclear bodies (PML-NBs) to stimulate the induction of innate immune defences against herpes simplex virus 1 (HSV-1) infection. Following the activation of innate immune signalling, HIRA localized at PML-NBs in a Janus-Associated Kinase (JAK), Cyclin Dependent Kinase (CDK), and Sp100-dependent manner. RNA-seq analysis revealed that HIRA promoted the transcriptional upregulation of a broad repertoire of host genes that regulate innate immunity to HSV-1 infection, including those involved in MHC-I antigen presentation, cytokine signalling, and interferon stimulated gene (ISG) expression. ChIP-seq analysis revealed that PML, the principle scaffolding protein of PML-NBs, was required for the enrichment of HIRA onto ISGs, identifying a role for PML in the HIRA-dependent regulation of innate immunity to virus infection. Our data identifies independent roles for HIRA in the intrinsic silencing of viral gene expression and the induction of innate immune defences to restrict the initiation and propagation of HSV-1 infection, respectively. These intracellular host defences are antagonized by the HSV-1 ubiquitin ligase ICP0, which disrupts the stable recruitment of HIRA to infecting viral genomes and PML-NBs at spatiotemporally distinct phases of infection. Our study highlights the importance of histone chaperones to regulate multiple phases of intracellular immunity to virus infection, findings that are likely to be highly pertinent in the cellular restriction of many clinically important viral pathogens.
2019-03-12 | GSE128173 | GEO
Project description:Many bacterial infections are hard to treat and tend to relapse, possibly due to the presence of antibiotic-tolerant persisters that are considered dormant cells when bacteria are grown in laboratory medium. Non-growing persisters also form following uptake of Salmonella by macrophages but their nature is little understood. Here we show that Salmonella persisters arising during macrophage infection maintain an active state. Persisters reprogram macrophages by means of effectors secreted by the SPI-2 Type 3 Secretion System (T3SS), thereby dampening pro-inflammatory innate immune responses and inducing anti-inflammatory macrophage polarisation. Reprogramming allows non-growing Salmonella to survive for extended periods in their host. Persisters undermining the host immune defences might confer an advantage to the pathogen during relapse once the antibiotic pressure is relieved.
2018-12-07 | GSE104785 | GEO
Project description:ARID1A regulates condensin II distribution and chromosomal partition
| PRJNA491495 | ENA
Project description:Salmonella persisters undermine host immune defences during antibiotic treatment
| PRJNA413814 | ENA
Project description:In this report we have discovered a new function of BRG1 during hormone-mediated gene repression. The ATPase BRG1 without the other subunits of the BAF complex is recruited by the hormone receptor to genomic sites marked by the pioneering factor FOXA1, where it remodels the target chromatin by interacting with linker histone H1.2 facilitating its deposition.
2016-07-11 | GSE83785 | GEO
Project description:Hormone dependent activation of enhancers includes histone hyperacetylation and mediator recruitment. Histone hyperacetylation is often explained by a bimodal switch mod-el, where histone deacetylases (HDACs) disassociates from chromatin and histone acetyl transferases (HATs) are recruited. This model builds on decades of research on steroid re-ceptor regulation of transcription. We have used a genomics approach to study enhancer hyperacetylation by the thyroid hormone receptor (TR) and present a revised model. 1) at poised constitutively TR bound enhancers, HATs occupy chromatin irrespective of thyroid hormone (T3) levels, whereas HDAC occupancy is regulated by T3, suggesting that HDACs functions as a histone acetylation rheostat. 2) at enhancers established in a T3 dependent manner, TR is recruited to chromatin together with HATs. 3) a number of enhancers are hy-peracetylated secondary to TR activation. Collectively, this demonstrates various mechanisms controlling hormone dependent transcription and adds significant details to the otherwise simple bimodal switch model.
2019-07-01 | GSE128535 | GEO
Project description:When mimicry imposes costs on models, selection may drive the model's phenotype to evolve away from its mimic. For example, brood parasitism often drives hosts to diversify in egg appearance among females within a species, making mimetic parasitic eggs easier to detect. However, when a single parasite species exploits multiple host species, parasitism could also drive host egg evolution away from other co-occurring hosts, to escape susceptibility to their respective mimics. This hypothesis predicts that sympatric hosts of the same parasite should partition egg phenotypic space (defined by egg colour, luminance and pattern) among species to avoid one another. We show that eggs of warbler species parasitized by the cuckoo finch Anomalospiza imberbis in Zambia partition phenotypic space much more distinctly than do eggs of sympatric but unparasitized warblers. Correspondingly, cuckoo finch host-races better match their own specialist host than other local host species. In the weaver family, parasitized by the diederik cuckoo Chrysococcyx caprius, by contrast, parasitized species were more closely related and overlapped extensively in phenotypic space; correspondingly, cuckoos did not match their own host better than others. These results suggest that coevolutionary arms races between hosts and parasites may be shaped by the wider community context in which they unfold.
| S-EPMC5443948 | biostudies-literature
Project description:ARID1A regulates condensin II distribution and chromosomal partition [HiC]
| PRJNA491601 | ENA