Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA320249 | ENA |
REPOSITORIES: ENA
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Project description:As most of the mitochondrial proteome is encoded in the nucleus, mitochondrial functions critically depend on nuclear gene expression and bidirectional mito-nuclear communication. However, mitochondria-to-nucleus communication pathways are incompletely understood. Here, we identify G-Protein Pathway Suppressor 2 (GPS2) as a mediator of mitochondrial retrograde signaling and a key transcriptional activator of nuclear-encoded mitochondrial genes in mammals. GPS2 regulated translocation from mitochondria to nucleus is essential for the transcriptional activation of the nuclear stress response to mitochondrial depolarization and for supporting basal mitochondrial biogenesis in differentiating adipocytes and in brown adipose tissue from mice. In the nucleus, GPS2 recruitment to target gene promoters regulates histone H3K9 demethylation and RNA Polymerase II (POL2) activation through inhibition of Ubc13-mediated ubiquitination. These findings, together, reveal an unexpected layer of regulation of mitochondrial gene transcription, uncover a novel direct mitochondria-nuclear communication pathway and indicate that GPS2 retrograde signaling is a key component of the mitochondrial stress response in mammals.
2018-03-21 | GSE80994 | GEO
Project description:As most of the mitochondrial proteome is encoded in the nucleus, mitochondrial functions critically depend on nuclear gene expression and bidirectional mito-nuclear communication. However, mitochondria-to-nucleus communication pathways are incompletely understood. Here, we identify G-Protein Pathway Suppressor 2 (GPS2) as a mediator of mitochondrial retrograde signaling and a key transcriptional activator of nuclear-encoded mitochondrial genes in mammals. GPS2 regulated translocation from mitochondria to nucleus is essential for the transcriptional activation of the nuclear stress response to mitochondrial depolarization and for supporting basal mitochondrial biogenesis in differentiating adipocytes and in brown adipose tissue from mice. In the nucleus, GPS2 recruitment to target gene promoters regulates histone H3K9 demethylation and RNA Polymerase II (POL2) activation through inhibition of Ubc13-mediated ubiquitination. These findings, together, reveal an unexpected layer of regulation of mitochondrial gene transcription, uncover a novel direct mitochondria-nuclear communication pathway and indicate that GPS2 retrograde signaling is a key component of the mitochondrial stress response in mammals.
2018-03-21 | GSE80993 | GEO
Project description:As most of the mitochondrial proteome is encoded in the nucleus, mitochondrial functions critically depend on nuclear gene expression and bidirectional mito-nuclear communication. However, mitochondria-to-nucleus communication pathways are incompletely understood. Here, we identify G-Protein Pathway Suppressor 2 (GPS2) as a mediator of mitochondrial retrograde signaling and a key transcriptional activator of nuclear-encoded mitochondrial genes in mammals. GPS2 regulated translocation from mitochondria to nucleus is essential for the transcriptional activation of the nuclear stress response to mitochondrial depolarization and for supporting basal mitochondrial biogenesis in differentiating adipocytes and in brown adipose tissue from mice. In the nucleus, GPS2 recruitment to target gene promoters regulates histone H3K9 demethylation and RNA Polymerase II (POL2) activation through inhibition of Ubc13-mediated ubiquitination. These findings, together, reveal an unexpected layer of regulation of mitochondrial gene transcription, uncover a novel direct mitochondria-nuclear communication pathway and indicate that GPS2 retrograde signaling is a key component of the mitochondrial stress response in mammals.
2018-03-21 | GSE80992 | GEO
Project description:As most of the mitochondrial proteome is encoded in the nucleus, mitochondrial functions critically depend on nuclear gene expression and bidirectional mito-nuclear communication. However, mitochondria-to-nucleus communication pathways are incompletely understood. Here, we identify G-Protein Pathway Suppressor 2 (GPS2) as a mediator of mitochondrial retrograde signaling and a key transcriptional activator of nuclear-encoded mitochondrial genes in mammals. GPS2 regulated translocation from mitochondria to nucleus is essential for the transcriptional activation of the nuclear stress response to mitochondrial depolarization and for supporting basal mitochondrial biogenesis in differentiating adipocytes and in brown adipose tissue from mice. In the nucleus, GPS2 recruitment to target gene promoters regulates histone H3K9 demethylation and RNA Polymerase II (POL2) activation through inhibition of Ubc13-mediated ubiquitination. These findings, together, reveal an unexpected layer of regulation of mitochondrial gene transcription, uncover a novel direct mitochondria-nuclear communication pathway and indicate that GPS2 retrograde signaling is a key component of the mitochondrial stress response in mammals.
2018-03-21 | GSE80990 | GEO
Project description:Mitochondrial retrograde signaling in mammals is mediated by the transcriptional cofactor GPS2 via direct mitochondria-to-nucleus translocation
| PRJNA320244 | ENA
Project description:Mitochondrial retrograde signaling in mammals is mediated by the transcriptional cofactor GPS2 via direct mitochondria-to-nucleus translocation [ChIP-seq]
| PRJNA320248 | ENA
Project description:Mitochondrial retrograde signaling in mammals is mediated by the transcriptional cofactor GPS2 via direct mitochondria-to-nucleus translocation [RNA-seq]
| PRJNA320247 | ENA
Project description:Strigolactones (SL) are a new class of plant hormones with a broad range of roles in symbiosis, germination and developmental regulation. The well-characterized signaling pathway for SL involves the canonical signaling component MAX2. Here we identified a novel, MAX2-independent SL signaling mechanism, which initiates in mitochondria, signals to the nucleus and regulates root development. By a forward genetic approach, we identified the SL-insensitive pig1 mutant, which altered the kinetic properties of the mitochondrial pyruvate dehydrogenase complex. SL has an unknown target in mitochondria, where it uncouples respiration. This leads to metabolic aberrations, mitochondria-to-nucleus retrograde signaling upregulating transcription of mitochondrial dysfunction genes and downregulating auxin-regulated genes. SL-triggered mitochondrial uncoupling is communicated to the nucleus via cleavage and translocation of the ER-localized transcription factor ANAC017. These observations establish a novel mechanism for SL signaling emanating from mitochondria and regulating development.
2022-04-18 | GSE200634 | GEO
Project description:Mitochondria are crucial for plant viability and are able to communicate information on their functional status to the cellular nucleus via retrograde signalling, thereby affecting gene expression. It is currently unclear if retrograde signalling in response to constitutive mitochondrial biogenesis defects is mediated by the same pathways as those triggered during acute mitochondrial dysfunction. Furthermore, it is unknown if retrograde signalling can effectively improve plant performance when mitochondrial function is constitutively impaired. Here we show that retrograde signalling in mutants defective in mitochondrial proteins RNA polymerase rpotmp or prohibitin atphb3 can be suppressed by knocking out the transcription factor ANAC017. Genome-wide RNA-seq expression analysis revealed that ANAC017 is almost solely responsible for the most dramatic transcriptional changes common to rpotmp and atphb3 mutants, regulating both classical marker genes such as alternative oxidase 1a (AOX1a) and also previously-uncharacterised DUF295 genes that appear to be new retrograde markers. In contrast, ANAC017 does not regulate intra-mitochondrial gene expression or transcriptional changes unique to either rpotmp or atphb3 genotype, suggesting the existence of currently unknown signalling cascades. The data show that the role of ANAC017 extends beyond common retrograde transcriptional responses and affects downstream protein abundance and enzyme activity of alternative oxidase, as well as steady state energy metabolism in atphb3 plants. Furthermore, detailed growth analysis revealed that ANAC017-dependent retrograde signalling provides benefits for growth and productivity in plants with mitochondrial defects. In conclusion, ANAC017 plays a key role in both biogenic and operational mitochondrial retrograde signalling, and improves plant performance when mitochondrial function is constitutively impaired.
2016-07-28 | E-MTAB-4655 | biostudies-arrayexpress
Project description:Hypoxia is one of the main driving forces that results in poor outcomes and drug resistance in hepatocellular carcinoma (HCC). As the critical cellular oxygen sensor, mitochondria respond to hypoxic stress by sending retrograde signals to the nucleus that initiate adaptive metabolic responses and maintain the survival of HCC cells. Increasing evidence suggested autophagy contributes to sustain mitochondrial metabolic and quality control. Understanding how mitochondria communicate with the nucleus and alter transcription may provide promising targets for HCC treatment. In this study, we found mitochondrial undergoes selective degradation by autophagy under hypoxia. Furthermore, autophagy-activated HDAC6 not only promoted the nuclear translocation of b-catenin but also increased the affinity of b-catenin to the transcription repressor chicken ovalbumin upstream promoter-transcription factor 2 (COUP-TF II;), which suppressed mitochondrial oxidative phosphorylation-related genes transcription. Our data showed that autophagy served as a critical mediator of integrating mitochondrial energy metabolism and nuclear transcription. HDAC6 may be a potential target for reducing the survival of HCC cells by interrupting mitochondrial–nuclear crosstalk
2021-11-05 | GSE186801 | GEO