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MRNA profiling of Pontin WT and RA under glucose starvation

ABSTRACT: mRNA profiling of Pontin WT and RA under glucose starvation

PROVIDER: PRJNA533787 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8931642_1.fastq.gz	Fastqsanger.gz
	SRR8931642_2.fastq.gz	Fastqsanger.gz
	SRR8931643_1.fastq.gz	Fastqsanger.gz
	SRR8931643_2.fastq.gz	Fastqsanger.gz
	SRR8931644_1.fastq.gz	Fastqsanger.gz

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mRNA profiling of Pontin WT and RA under glucose starvation

Project description:To determine which genes are affected by methylated Pontin, we performed RNA-sequencing (RNA-seq) in Pontin WT and RA MEFs after glucose starvation.

2020-10-26 | GSE130069 | GEO

Genome binding/occupancy profiling of methylated Pontin under glucose starvation

Project description:To determine where methylated Pontin is recruited, we performed ChIP-sequencing (ChIP-seq) in WT MEFs after glucose starvation.

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Genome binding/occupancy profiling of methylated Pontin under glucose starvation

Project description:Genome binding/occupancy profiling of methylated Pontin under glucose starvation

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Pontin Functions as A Transcriptional Co-activator for Retinoic Acid-induced HOX Gene Expression [ChIP-seq]

Project description:Pontin is a AAA+ ATPase protein that has functions in various biological contexts including gene transcription regulation, chromatin remodeling, DNA damage sensing and repair, as well as assembly of protein and ribonucleoprotein complexes. Pontin is known to regulate the transcription of several important signaling pathways, including Wnt signaling. However, its role in early embryonic signaling regulation remains unclear. Retinoic acid (RA) signaling plays a central role in vertebrate development. Using an in vivo biotin tagging technology, we mapped the genome-wide binding pattern of Pontin before and after RA-induced differentiation in the pluripotent embryo carcinoma cell line NTEAR-2. Biotin ChIP-seq revealed significant changes in genome-wide Pontin binding sites upon RA stimulation. We also identified a substantial amount of overlapping binding peaks between Pontin and RARα, especially on all of the HOX gene loci (A-D clusters). Pontin knockdown experiments showed that its chromatin binding at the HOX gene clusters is required for RA-induced HOX gene expression. Furthermore, we performed Global Run-On sequencing (GRO-seq) to map de novo transcripts genome-wide and found that Pontin knockdown significantly diminished nascent HOX gene transcripts, indicating that Pontin regulates HOX gene expression at the transcriptional level. Finally, proteomic analysis demonstrated that Pontin associates with chromatin organization/remodeling complexes and various other functional complexes. Altogether, we have demonstrated that Pontin is a critical transcriptional co-activator for RA-induced HOX gene activation.

2021-06-16 | GSE162360 | GEO

Pontin Functions as A Transcriptional Co-activator for Retinoic Acid-induced HOX Gene Expression [GRO-seq]

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Project description:The adaptation of tumor cells to metabolic stress is crucial for tumor development. We demonstrate that the translation of NRF2, a master regulator of antioxidant response, is controlled by the OGDH-METTL3 axis in melanoma for glucose starvation adaptation. To elucidate the regulatory mechanism of the OGDH-METTL3 axis during glucose starvation, we conducted co-immunoprecipitation and mass spectrometry analysis to identify the binding partner of OGDH that governs both the OGDH-METTL3 axis and tumor cell adaptation to glucose deprivation.

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MANF facilitates breast cancer cell survival under glucose starvation via PRKN-mediated mitophagy regulation

Project description:Glucose shortage can lead to ROS accumulation and thus induce mitochondrial damage in breast cancer (BC) cells. However, the role of mitophagy in cancer cells under glucose starvation remains unclear. Here, we showed that mesencephalic astrocyte-derived neurotrophic factor (MANF)-mediated mitophagy facilitates BC cell survival under glucose starvation. MANF-mediated mitophagy also promotes fatty acid oxidation in glucose-starved BC cells. Moreover, under glucose starvation, SENP1-mediated de-SUMOylation of MANF increases cytoplasmic MANF expression through the inhibition of MANF’s nuclear translocation and hence renders mitochondrial distribution of MANF. MANF mediates mitophagy by binding to parkin RBR E3 ubiquitin protein ligase (PRKN), a key mitophagy regulator, in the mitochondria. Under glucose starvation, protein oxidation inhibits PRKN activity; nevertheless, CXXC motif of MANF alleviates protein oxidation in RING II-domain of PRKN and restores its E3 ligase activity. Furthermore, MANF–PRKN interactions are essential for BC tumor growth and metastasis. High MANF expression predicts poor outcomes in patients with BC. Our results provide a mechanistic explanation for the prosurvival role of MANF-mediated mitophagy in BC cells under glucose starvation and may point to targetable vulnerabilities.

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