Functional dissection of the regulatory mechanism of the atypical AP-1-like transcription factor, Yap1, in Cryptococcus neoformans
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ABSTRACT:
PROVIDER: PRJNA563833 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10065422_1.fastq.gz | Fastqsanger.gz | |||
| SRR10065422_2.fastq.gz | Fastqsanger.gz | |||
| SRR10065423_1.fastq.gz | Fastqsanger.gz | |||
| SRR10065423_2.fastq.gz | Fastqsanger.gz | |||
| SRR10065424_1.fastq.gz | Fastqsanger.gz |
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Project description:AP-1 like transcription factors play evolutionarily conserved roles in oxidative stress responses as redox sensors in eukaryotes. In this study, we aim to elucidate the regulatory mechanism of an atypical yeast AP-1 like protein, Yap1, in the stress response and virulence of Cryptococcus neoformans. YAP1 expression was induced not only by oxidative stresses, such as H2O2 and diamide, but also by other environmental stresses, such as osmotic and membrane destabilizing stresses. Supporting these data, Yap1 was involved in osmotic and membrane stress responses as well as oxidative stress responses. Pleiotropic roles of Yap1 in diverse biological processes were supported by transcriptome analysis data showing that more than 162 genes are differentially regulated by Yap1. This analysis also provided a clue that Yap1 is involved in carbohydrate metabolism and indeed we found that Yap1 promotes cellular resistance to toxic cellular metabolites produced during glycolysis, such as methylglyoxal. Finally, we demonstrated that Yap1 played a minor role in survival of C. neoformans within hosts.
2019-11-07 | GSE136832 | GEO
Project description:YAP1 complexes separation with affinity purification (AP) coupled to BNPAGE
2023-03-04 | PXD030061 | Pride
Project description:We report that TNFalpha mediated dendritic cell priming via alterations in histone 3 lysine 4 trimethylation (H3K4me3) sustains lasting protective Th1/Th17 responses during invasive Cryptococcus neoformans pulmonary infection. Cryptococcus neoformans pulmonary infection results in increased global lung dendritic cell H3K4me3 over naive lung dendritic cells. Blockage of TNFalpha during Cryptococcus neoformans pulmonary infection results in decreased H3K4me3 at sites crucial to protective Th1/Th17 responses.
2018-08-15 | GSE118543 | GEO
Project description:In this project we investigated the topological composition of ternary complex PTPN14/LATS1/PTPN14. For this purpose, we performed affinity purification with Strep tag of Strep-HA YAP1 and subsequent XL reaction.
2023-03-04 | PXD039440 | Pride
Project description:Proteins which act as histone chaperones ensure genomic integrity during routine processes such as DNA replication and transcription as well as DNA repair upon damage. Herein, we identify a nuclear J domain protein, Dnj4, which interacts with histones 3 and 4 as well as Hsp71 as demonstrated in an AP-MS experiment suggesting that it integrates the heat shock chaperone machinery into histone chaperoning. In support of this, a deletion mutant lacking DNJ4 had higher levels of DNA damage than the wild type or complemented strains and was hypersensitive to DNA damaging agents. The transcriptional response to DNA damage in a mutant lacking DNJ4 was impaired. Genes related to DNA damage and iron homeostasis functions were up-regulated in the wild type strain in response to hydroxyurea treatment, however their up-regulation was either absent or reduced in a dnj4∆ mutant. Accordingly, excess iron rescued the mutant’s growth in response to hydroxyurea treatment. Iron homeostasis is crucial for virulence in Cryptococcus neoformans, however Dnj4 was found to be dispensable for virulence in a mouse model of cryptococcosis. Finally, we confirmed a conserved role of Dnj4 in histone chaperoning by expressing it in S. cerevisiae and showing that it disrupted endogenous histone chaperoning. Altogether, this study highlights the importance of a JDP co-chaperone in histone chaperoning in C. neoformans.
2021-12-15 | PXD028087 | Pride
Project description:We measured protein translation (by ribosome profiling) and RNA levels (by polyA-enriched RNA-seq) in Cryptococcus neoformans strain H99 and Cryptococcus neoformans strain JEC21. This is the first transcriptome-wide map of translation in this species complex.
2019-06-22 | GSE133125 | GEO
Project description:AP-1-like transcription factors play evolutionarily conserved roles as redox sensors in eukaryotic oxidative stress responses. In this study, we aimed to elucidate the regulatory mechanism of an atypical yeast AP-1-like protein, Yap1, in the stress response and virulence of Cryptococcus neoformansYAP1 expression was induced and involved not only by oxidative stresses, such as H2O2 and diamide, but also by other environmental stresses, such as osmotic and membrane-destabilizing stresses. Yap1 was distributed throughout both the cytoplasm and the nucleus under basal conditions and more enriched within the nucleus in response to diamide but not to other stresses. Deletion of the C-terminal cysteine-rich domain (c-CRD), where the nuclear export signal resides, increased nuclear enrichment of Yap1 under basal conditions and altered resistance to oxidative stresses but did not affect the role of Yap1 in other stress responses and cellular functions. As a potential upstream regulator of Yap1, we discovered that Mpk1 is positively involved, but Hog1 is mostly dispensable. Pleiotropic roles for Yap1 in diverse biological processes were supported by transcriptome data showing that 162 genes are differentially regulated by Yap1, with further analysis revealing that Yap1 promotes cellular resistance to toxic cellular metabolites produced during glycolysis, such as methylglyoxal. Finally, we demonstrated that Yap1 plays a minor role in the survival of C. neoformans within hosts.IMPORTANCE The human meningitis fungal pathogen, Cryptococcus neoformans, contains the atypical yeast AP-1-like protein Yap1. Yap1 lacks an N-terminal cysteine-rich domain (n-CRD), which is present in other fungal Yap1 orthologs, but has a C-terminal cysteine-rich domain (c-CRD). However, the role of c-CRD and its regulatory mechanism remain unknown. Here, we report that Yap1 is transcriptionally regulated in response to oxidative, osmotic, and membrane-destabilizing stresses partly in an Mpk1-dependent manner, supporting its role in stress resistance. The c-CRD domain contributed to the role of Yap1 only in resistance to certain oxidative stresses and azole drugs but not in other cellular functions. Yap1 has a minor role in the survival of C. neoformans in a murine model of systemic cryptococcosis.
| S-EPMC6887862 | biostudies-literature
Project description:In order to define YAP1-specific gene expression patterns in gastric cancer, the constitutively active mutant YAP1 (YAP1-S127A) was over-expressed in MKN45 gastric cancer cells. Defined gene expression signature was later used to stratify gastric cancer patients according to the presence of the YAP1-activated signature. Three groups of samples are included: 1. Mock control; 2. Vector control; 3. YAP-S127A expression. Gene expression profiles of YAP-S127A mutant-expressing cells were compared to that of mock and vector control. Experiments were done in MKN45 gastric cancer cells.
2013-10-01 | E-GEOD-41387 | biostudies-arrayexpress
Project description:Doxycycline-inducible YAP1 S127A-driven rhabdomyosarcoma (RMS) tumors, control skeletal muscle and regressed tumors following YAP1 normalization by doxycycline withdrawal were compared to determine the YAP1-regulated gene expression profile relevant to RMS formation. To characterize the role of YAP1 in embryonal RMS at the molecular level and identify a gene signature for YAP1 activity readout, we compared the gene expression profiles of our YAP1-driven ERMS with control donor skeletal muscle (SKM) and doxycycline-withdrawn regressing tumors by microarray (doxycycline withdrawal for 3 or 6 days; OFF3 and OFF6, respectively). We next extracted a list of genes regulated by YAP1 in our YAP1-driven ERMS tumors (TUM) versus the 3 other conditions: skeletal muscle control (SKM), Doxycycline-withdrawn 3 days (OFF3) and 6 days (OFF6). The overlap between the 3 lists identified a subset of 633 common upregulated genes, named the YAP1-ERMS_UP signature, as well as 249 common downregulated genes, termed the YAP1-ERMS_DOWN signature. Proliferative pathways and transcriptional targets of E2F factors were highlighted in the YAP1-ERMS_UP genes, while muscle differentiation and trancriptional targets of myogenic factors Myod1 and Mef2 were highlighted in the YAP1-ERMS_DOWN genes. Tumor regression conditions (OFF3 days; OFF6 days) as well as control muscle (CTL) were compared with tumors at day 0 of doxycycline withdrawal (TUM). 3 samples for each conditions were used.
2014-08-12 | E-GEOD-47198 | biostudies-arrayexpress
Project description:Proper mitochondrial function is critical for the ability of the fungal pathogen Cryptococcus neoformans to cause disease. Mitochondrial dysfunction of WT cells treated with antimycin A or L-DOPA, or on cells lacking Cir1 is evident from this dataset. These experiments revealed influences on transcript levels of genes encoding Fe-S cluster assembly components and the response to oxidative stress in Cryptococcus neoformans.
2024-04-07 | GSE222564 | GEO