Project description:By comparing data from the three cytolines (two cytoplsm donors and one nucleus donor) we identified key nuclear genes whose expression is modulated through the retrograde signaling pathways.
Project description:Using maize cytolines (same nucleus but different cytoplasms), our research adds a new facet to the paradigm explaining gene expression changes in response to heat stress in an effort to maintain the homeostasis, linking the response to the genetic divergence of the nuclear and organellar genomes.
Project description:Analysis of transcriptome response of norflurazon treated or untreated 5-day old whole seedlings with genotypes: Col6-3 (wild type), gun1-9 and MORF2 overexpression lines. GUN1 and MORF2 are involved in chloroplast-to-nucleus retrograde signaling. Results provide insight into the nuclear genes expression profile under control of GUN1 retrograde pathways and the regulation similarity between gun1-9 and MORF2 overexpression lines.
Project description:The cytopheno project studies cytoplasmic-nucleus interactions by characterizing cytolines (same nucleus but different cytoplasm, and conversely) at several levels (growth, germination, transcriptomic, proteomic, metabolomic) notably in response to nitrogen deficiency. For this project, there are 48 hybridizations performed as following, on leaf samples from hydroponically grown plants. bioadapt2011_cytopheno - bioadapt2011_cytopheno - Evaluation of the impact of nucleo-cytoplasmic co-adaptation disruptions on nuclear genome expression in Arabidopsis - Obtaining samples by hydroponic culture.
Project description:Retrograde signals emanate from the DNA-containing cell organelles (plastids and mitochondria) and control the expression of a large number of nuclear genes in response to environmental and developmental cues. GENOMES UNCOUPLED1 (GUN1) participating in multiple retrograde signaling pathways that collectively regulate the nuclear transcriptome. We used microarrays to further investigate the regulation of nuclear gene expression by PGE retrograde signals mediated by GUN1.
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.
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.
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.