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XCT is a novel regulator of chromatin functionally conserved across eukaryotes

ABSTRACT: XCT was originally identified due to the short circadian period observed in plants mutant for this gene. Proteins with homology to XCT are found across eukaryotes, but their molecular function is unknown. We have recently demonstrated that in Schizosaccharomyces pombe, the XCT ortholog Xap5 is a chromatin-associated protein that acts in a similar manner as the histone variant H2A.Z to suppress aberrant gene expression. Here, we demonstrate that although XCT and H2A.Z act in similar pathways to control plant development, XCT's role in the circadian clock is independent of H2A.Z.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE67813 | GEO | 2019/05/01

REPOSITORIES: GEO

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XAP5 CIRCADIAN TIMEKEEPER regulates RNA splicing and the circadian clock by genetically separable pathways

Project description:Regulators of post-transcriptional events, such as pre-mRNA splicing factors, are involved in controlling the pace of the circadian clock. However, in most cases the underlying mechanisms remain unclear. Previously, we have identified XAP5 CIRCADIAN TIMEKEEPER (XCT) as an Arabidopsis thaliana circadian clock regulator with uncharacterized molecular functions. To investigate a possible role for XCT in RNA splicing, we performed PacBio Isoform Sequencing (Iso-Seq) on wild-type Col-0, reduction-of-function allele xct-1, null allele xct-2, the complemented line xct-2 XCT and prl1-2 (a mutate with known defects in intron retention). We then performed differential splicing analysis on the Iso-Seq data using JunctionSeq R package. Our results indicate that xct mutants have transcriptome-wide pre-mRNA splicing defects, predominantly aberrant 3’ splice site selection. Expression of a genomic copy of XCT fully rescues those splicing defects.

2023-04-01 | GSE220902 | GEO

Inhibition of xCT Suppresses Melanoma progress

Project description:Tumor cells increase glutamate release through the cystine/glutamate transporter xCT to balance oxidative homeostasis in tumor cells and promote tumor progression. Here, we demonstrated that although inhibition of xCT either by pharmacological inhibitor (sulfasalazine, SAS), approved by FDA for inflammatory diseases, or genetic knockdown induced ROS-related death in melanoma cells. Taken together, our results reveal that inhibition of xCT by SAS is a promising therapeutic strategy for melanoma.

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Yeast X-Chromosome Associated Protein 5 (Xap5) Functions with H2A.Z to Suppress Aberrant Transcripts [ChIP-chip]

Project description:Comparison of occupancy profiling of Xap5 and H2A.Z/Pht1 in fission yeast. Agilent 60mer array was used to analyze DNA recovered by chromatin immunoprecipitation of Xap5 from fission yeast culture.

2014-07-01 | E-GEOD-46505 | biostudies-arrayexpress

Yeast X-Chromosome Associated Protein 5 (Xap5) Functions with H2A.Z to Suppress Aberrant Transcripts [ChIP-chip]

Project description:Comparison of occupancy profiling of Xap5 and H2A.Z/Pht1 in fission yeast.

2014-07-01 | GSE46505 | GEO

Role of the glial glutamate exchanger xCT in ventral hippocampus in resilience to stress

Project description:We demonstrate that stress differentially regulates glutamate homeostasis in the dorsal and ventral hippocampus and established a previously unknown role for the glial marker xCT in the homeostatic regulation of the ventral dentate gyrus (vDG) in stress resilience and antidepressant responses. We provide RNAseq roadmap for the stress-sensitive vDG and show that the transcription factor REST binds to xCT promoter in co-occupancy with the epigenetic marker H3K27acet, to negatively regulate xCT expression. Reduced xCT was also observed in a genetic mouse model of inherent susceptibility to depression. Pharmacologically modulating histone acetylation with next-generation therapeutics, such as acetyl-N-cysteine (NAC) or acetyl-L-carnitine (LAC), rapidly increased xCT reduction and activated a network that included mGlu2 receptors to prime an enhanced glutamate homeostasis that promoted stress resilience and antidepressant-like responses. Moreover, pharmacological xCT blockage counteracted NAC prophylactic effects. Anatomical (vDG) and cell-type specific (GFAP+) virus-overexpression mimicked the effects of pharmacological treatments in increasing stress resilience. These findings establish xCT as critical regulator of the glutamate system in a network with mGlu2 receptors. These studies also point to a role of histone acetylation as mediator of stress resilience.

2017-10-11 | GSE103435 | GEO

Genomic analysis of xCT-mediated regulatory network: identification of novel targets against AIDS-associated lymphoma

Project description:Kaposiâs sarcoma-associated herpesvirus (KSHV) is the etiological agent of primary effusion lymphoma (PEL), a rapidly progressing malignancy mostly arising in HIV-infected patients. Even under conventional chemotherapy, PEL continues to portend nearly 100% mortality within several months, which urgently requires novel therapeutic strategies. We have previously demonstrated that targeting xCT, an amino acid transporter for cystine/glutamate exchange, induces significant PEL cell apoptosis through regulation of multiple host and viral factors. More importantly, one of xCT selective inhibitors, Sulfasalazine (SASP), effectively prevents PEL tumor progression in an immune-deficient xenograft model. In the current study, we use Illumina microarray to explore the genomic gene profile altered by SASP treatment within 3 KSHV+ PEL cell-lines, and discover that many genes involved in oxidative stress/antioxidant defense system, apoptosis/anti-apoptosis/cell death, and cellular response to unfolded proteins/topologically incorrect proteins are potentially regulated by xCT. We further functionally validate 2 downstream candidates, OSGIN1 (Oxidative stress-induced growth inhibitor 1) and XRCC5 (X-ray repair cross-complementing protein 5), their relationship with PEL cell survival/proliferation and chemoresistance, respectively. Together, our data indicate that targeting these xCT-regulated novel downstream genes may help devise promising therapeutic strategies against PEL and/or other AIDS-related lymphoma. 3 KSHV PEL cell lines were treated with xCT selective inhibitor Sulfasalazine (SASP) and the gene expression signature was compared to that of untreated cells

2015-11-23 | E-GEOD-65418 | biostudies-arrayexpress

Microvirga tunisiensis strain:XCT-34

Project description:Microvirga tunisiensis strain:XCT-34 Genome sequencing

| PRJNA643673 | ENA

Inhibition of xCT Suppresses Melanoma progress

Project description:Inhibition of xCT Suppresses Melanoma progress

| PRJNA701281 | ENA

Genomic analysis of xCT-mediated regulatory network: identification of novel targets against AIDS-associated lymphoma

Project description:Kaposi’s sarcoma-associated herpesvirus (KSHV) is the etiological agent of primary effusion lymphoma (PEL), a rapidly progressing malignancy mostly arising in HIV-infected patients. Even under conventional chemotherapy, PEL continues to portend nearly 100% mortality within several months, which urgently requires novel therapeutic strategies. We have previously demonstrated that targeting xCT, an amino acid transporter for cystine/glutamate exchange, induces significant PEL cell apoptosis through regulation of multiple host and viral factors. More importantly, one of xCT selective inhibitors, Sulfasalazine (SASP), effectively prevents PEL tumor progression in an immune-deficient xenograft model. In the current study, we use Illumina microarray to explore the genomic gene profile altered by SASP treatment within 3 KSHV+ PEL cell-lines, and discover that many genes involved in oxidative stress/antioxidant defense system, apoptosis/anti-apoptosis/cell death, and cellular response to unfolded proteins/topologically incorrect proteins are potentially regulated by xCT. We further functionally validate 2 downstream candidates, OSGIN1 (Oxidative stress-induced growth inhibitor 1) and XRCC5 (X-ray repair cross-complementing protein 5), their relationship with PEL cell survival/proliferation and chemoresistance, respectively. Together, our data indicate that targeting these xCT-regulated novel downstream genes may help devise promising therapeutic strategies against PEL and/or other AIDS-related lymphoma.

2015-11-23 | GSE65418 | GEO

mTORC2 regulates amino acid metabolism in cancer by phosphorylation of the cystine-glutamate antiporter xCT

Project description:Mutations in cancer reprogram amino acid metabolism to drive tumor growth, but the molecular mechanisms are not well understood. Using an unbiased proteomic screen, we identified mTORC2 as a critical regulator of amino acid metabolism in cancer via phosphorylation of the cystine-glutamate antiporter xCT. mTORC2 phosphorylates serine 26 at the cytosolic N-terminus of xCT, inhibiting its activity. Genetic inhibition of mTORC2, or pharmacologic mTOR kinase inhibition, promotes glutamate secretion, cystine uptake and incorporation into glutathione linking growth factor receptor signaling with amino acid uptake and utilization. These results identify an unanticipated mechanism of amino acid metabolic reprogramming in cancer, enabling tumor cells to adapt to changing environmental conditions.

2017-06-28 | PXD006461 | Pride

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