Ontology highlight
ABSTRACT:
PROVIDER: PRJNA938293 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23606907_1.fastq.gz | Fastqsanger.gz | |||
| SRR23606907_2.fastq.gz | Fastqsanger.gz | |||
| SRR23606908_1.fastq.gz | Fastqsanger.gz | |||
| SRR23606908_2.fastq.gz | Fastqsanger.gz | |||
| SRR23606909_1.fastq.gz | Fastqsanger.gz |
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Project description:We compare the phosphoproteome analysis of Cytospora chrysosperma wild type and CcPmk1 deletion mutant, which can help us to identify the putative regulation pattern of CcPmk1 through protein phosphorylation.
2022-10-14 | PXD032206 | Pride
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Project description:Cytospora chrysosperma CFL2056 Standard Draft genome sequencing
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Project description:Serum response factor (SRF) is a ubiquitously expressed transcription factor that is essential for brain development and function. SRF activity is controlled by two competing classes of coactivators, myocardin-related transcription factors (MRTF) and ternary complex factors, which introduce specificity into gene expression programs. Here, we explored the MRTF-mediated regulatory mechanism in mouse cortical neurons. Using gene-reporter assays and pharmacological and genetic approaches in isolated mouse cortical neurons, we found that cyclase-associated protein 1 (CAP1) repressed neuronal MRTF-SRF activity. CAP1 promoted cytosolic retention of MRTF by controlling cytosolic G-actin levels that required its helical folded domain and its CARP domain. This function of CAP1 was not redundant with that of its homolog CAP2 and was independent of cofilin1 and actin-depolymerizing factor. Deep RNA sequencing and mass spectrometry in cerebral cortex lysates from CAP1 knockout (CAP1-KO) mice supported the in vivo relevance for the CAP1-actin-MRTF-SRF signaling axis. Our study identified CAP1 as a repressor of neuronal gene expression and led to the identification of likely MRTF-SRF target genes in the developing cerebral cortex, whose dysregulation may contribute to impaired formation of neuronal networks in CAP1-KO mice. Together with our previous studies that implicated CAP1 in actin dynamics in axonal growth cones or excitatory synapses, we established CAP1 as a crucial actin regulator in neurons.
2024-03-22 | GSE262154 | GEO
Project description:<p>Pmk1, a highly conserved pathogenicity-related mitogen-activated protein kinase (MAPK) in pathogenic fungi, is phosphorylated and activated by MAP2K and acts as a global regulator of fungal infection and invasive growth by modulating downstream targets. However, the hierarchical CcPmk1 regulatory network in <em>Cytospora chrysosperma</em>, the main causal agent of canker disease in many woody plant species, is still unclear. In this study, we analyzed and compared the phosphoproteomes and metabolomes of Δ<em>CcPmk1</em> and wild-type strains and identified pathogenicity-related downstream targets of CcPmk1. We found that CcPmk1 could interact with the downstream homeobox transcription factor CcSte12 and affect its phosphorylation. In addition, the Δ<em>CcSte12</em> displayed defective phenotypes that were similar to yet not identical to that of the Δ<em>CcPmk1</em> and included significantly reduced fungal growth, conidiation and virulence. Remarkably, CcPmk1 could phosphorylate proteins translated from a putative secondary metabolism-related gene cluster, which is specific to <em>C. chrysosperma</em>, and the phosphorylation of several peptides was completely abolished in the Δ<em>CcPmk1</em>. Functional analysis of the core gene (<em>CcPpns1</em>) in this gene cluster revealed its essential roles in fungal growth and virulence. Metabolomic analysis showed that amino acid metabolism and biosynthesis of secondary metabolites, lipids, and lipid-like molecules significantly differed between wild type and Δ<em>CcPmk1</em>. Importantly, most of the annotated lipids and lipid-like molecules were significantly downregulated in the Δ<em>CcPmk1</em> compared to the wild type. Collectively, these findings suggest that CcPmk1 may regulate a small number of downstream master regulators to control fungal growth, conidiation and virulence in <em>C. chrysosperma</em>.</p><p><br></p><p><strong>Data availability:</strong></p><p>The proteomics data have been deposited into the ProteomeXchange Consortium via the PRIDE partner repository with the data set identifier <a href='https://www.ebi.ac.uk/pride/archive/projects/PXD032206' rel='noopener noreferrer' target='_blank'>PXD032206</a>.</p>
2022-07-11 | MTBLS4463 | MetaboLights
Project description:Constitutive overexpression of the Mdr1 efflux pump is an important mechanism of acquired drug resistance in the yeast Candida albicans. The zinc cluster transcription factor Mrr1 is a central regulator of MDR1 expression, but other transcription factors have also been implicated in MDR1 regulation. To better understand how MDR1-mediated drug resistance is achieved in this important fungal pathogen, we studied the interdependence of Mrr1 and two other MDR1 regulators, Upc2 and Cap1, in the control of MDR1 expression. A mutated, constitutively active Mrr1 could upregulate MDR1 and confer drug resistance in the absence of Upc2 or Cap1. On the other hand, Upc2 containing a gain-of-function mutation only slightly activated the MDR1 promoter, and this activation depended on the presence of a functional MRR1 gene. In contrast, a C-terminally truncated, activated form of Cap1 could upregulate MDR1 in a partially Mrr1-independent fashion. The induction of MDR1 expression by toxic chemicals occurred independently of Upc2, but required the presence of Mrr1 and also partially depended on Cap1. Transcriptional profiling and in vivo DNA binding studies showed that a constitutively active Mrr1 binds to and upregulates most of its direct target genes in the presence or absence of Cap1. Therefore, Mrr1 and Cap1 cooperate in the environmental induction of MDR1 expression in wild-type C. albicans, but gain-of-function mutations in either of the two transcription factors can independently mediate efflux pump overexpression and drug resistance.
2011-07-01 | GSE23532 | GEO
Project description:To investigate the roles of Sfp1, we used a whole-genome DNA microarray to compare gene expression patterns between the sfp1-deleted and wild-type strains. Among the upregulated genes, a subset of genes is involved in oxidative stress response, including CAP1, SSK1, and SHO1. The CAP1 gene product is a bZip transcription factor involving in regulation of antioxidant gene expression. The SSK1 and SHO1 gene encodes a response regulator of two-component system and an adaptor protein in the Hog1 MAPK signaling pathway, respectively. Moreover, the sfp1-deleted mutant also exhibited an upregulation of genes encoding various antioxidants and enzymes controlling the cellular redox state, especially components of the glutathione system. Noticeably, 8 of the 21 upregulated glutathione-related genes (GCS1, GTT11, YCF1, CYS3, CIP1, EBP1, IFD6, and OYE32) are controlled by Cap1. This result raises a possibility that Sfp1 is involved in C. albicans oxidative stress response and somehow coordinately regulates these glutathione-related genes with Cap1.
2019-06-20 | GSE127184 | GEO