Total RNA-seq upon degradation of OGT by siRNA
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB78519 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR13430770_1.fastq.gz | Fastqsanger.gz | |||
| ERR13430770_2.fastq.gz | Fastqsanger.gz | |||
| ERR13430771_1.fastq.gz | Fastqsanger.gz | |||
| ERR13430771_2.fastq.gz | Fastqsanger.gz | |||
| ERR13430772_1.fastq.gz | Fastqsanger.gz |
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Project description:Evaluation of change in gene expression upon degradation of OGT by siRNA
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Project description:O-linked N-acetylglucosamine (O-GlcNAc ) transferase (OGT) activity is essential for embryonic stem (ES) cell viability and mouse development. OGT is present in both cytoplasm and nucleus of different cell types and mediates serine or threonine glycosylation. The Ogt gene locus resides on the X-chromosome and its activity is required for the viability of male ES cells. Using Ogt conditional knock out (KO) ES cells it was shown the failure of establishing stable KO ES clones further suggesting that Ogt activity is required for ES cell self-renewal and pluripotency. For understanding these changes, we performed global gene expression upon silencing of Ogt mediated by esiRNA in mouse Embryonic Stem Cells. Total RNA was extracted from E14 ES cells (derived from Ola129 mice) transiently transfected with Ogt specific and control esiRNA oligos 48 hrs. post-transfection.
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Project description:This study aimed to elucidate the spatiotemporal expression pattern of O-GlcNAc transferase (OGT) and its catalyzed O-GlcNAc modification in ovarian tissues, and to investigate their specific functions in ovarian granulosa cells. To this end, high-throughput RNA sequencing was performed to analyze genome-wide transcriptional changes following OGT knockdown in the human ovarian granulosa cell line KGN. Two specific siRNAs targeting OGT (siOGT1 and siOGT2) and a negative control siRNA (siNC) were designed. Each group included two biological replicates, resulting in a total of six transcriptomic libraries. Sequencing was carried out on the Illumina NovaSeq 6000 platform with paired-end 150-bp reads. By comparing the siOGT-treated groups with the siNC control group, 300 and 487 differentially expressed genes (DEGs) were identified in the siOGT1 and siOGT2 groups, respectively, with 176 DEGs overlapping between the two groups. Pathway enrichment analysis indicated that OGT knockdown may affect pathways related to immune defense response, cellular reaction to external stimuli, and cytokine-mediated signaling. This dataset provides a transcriptomic profile of ovarian granulosa cells under OGT interference and serves as a key resource for further investigation into the regulatory mechanisms of the OGT/O-GlcNAc axis in ovarian physiology and pathology.
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Project description:O-linked β-N-acetylglucosamine (O-GlcNAc) transferase (OGT) is the sole enzyme that catalyzes all O-GlcNAcylation reactions intracellularly. Previous investigations have found that OGT levels oscillate during the cell division process. Specifically, OGT abundance is downregulated during mitosis, but the underlying mechanism is lacking. Here we demonstrate that OGT is ubiquitinated by the ubiquitin E3 ligase, anaphase promoting complex/cyclosome (APC/C)-cell division cycle 20 (Cdc20). We show that APC/CCdc20 interacts with OGT through a conserved destruction box (D-box): Arg-351/Leu-354, the abrogation of which stabilizes OGT. As APC/CCdc20-substrate binding is often preceded by a priming ubiquitination event, we also used mass spectrometry and mapped OGT Lys-352 to be a ubiquitination site, which is a prerequisite for OGT association with APC/C subunits. Interestingly in The Cancer Genome Atlas, R351C is a uterine carcinoma mutant, suggesting that mutations of the D-box are linked with tumorigenesis. Paradoxically, we found that both R351C and the D-box mutants (R351A/L354A) inhibit uterine carcinoma in mouse xenograft models, probably due to impaired cell division and proliferation. In sum, we propose a model where OGT Lys-352 ubiquitination primes its binding with APC/C, and then APC/CCdc20 partners with OGT through the D-box for its mitotic destruction. Our work not only highlights the key mechanism that regulates OGT during the cell cycle, but also reveals the mutual coordination between glycosylation and the cell division machinery.
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Project description:Every year, about 18 million babies are born from mothers with gestational diabetes mellitus (GDM). While diabetic symptoms usually resolve after delivery, lasting complications can occur for both mother and child, including fetal overgrowth, type 2 diabetes (T2D), cardiovascular diseases, and obesity. The rapid progression of GDM is unique to pregnancies, and likely arises from placental dysfunction. Indeed, stress, nutrition and fetal gender are thought to trigger changes in placental endocrine function, including metabolic hormones and inflammatory cytokines, potentially causing GDM. Nutrient-sensing O-GlcNAcylation and its enzyme O-GlcNAc Transferase (OGT, X-linked) has been previously identified as a placental biomarker of maternal stress particularly deleterious for male offspring. Thus, we wondered whether O-GlcNAcylation participate in GDM development in a sex-dependent manner. After demonstrating that OGT is largely downregulated in male GDM compared to healthy placentas, we knocked down OGT in male trophoblastic cells. We observed changes in placental hormones, cytokines and nutrient-sensing pathways, correlating with previously demonstrated disruption in GDM placentas. Altogether, this study demonstrates that OGT and O-GlcNAcylation are partly responsible for changes observed in GDM placenta and might be the cause of sexual dimorphism observed in this pathology.
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