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Plant organelles modulate nuclear gene expression

ABSTRACT: Maize cytolines provide key nuclear genes that are under the control of retrograde signaling pathways in plants

PROVIDER: PRJEB11473 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR1084200_1.fastq.gz	Fastqsanger.gz
	ERR1084200_2.fastq.gz	Fastqsanger.gz
	ERR1084201_1.fastq.gz	Fastqsanger.gz
	ERR1084201_2.fastq.gz	Fastqsanger.gz
	ERR1084202_1.fastq.gz	Fastqsanger.gz

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Project description:Maize cytolines provide key nuclear genes that are under the control of retrograde signaling pathways in plants

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Maize cytolines provide key nuclear genes that are under the control of retrograde signaling pathways in plants

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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.

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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.

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Retrograde signalling during caused by heritable mitochondrial dysfunction is partly mediated by ANAC017 and improves plant performance.

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.

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Mitochondrial retrograde signaling in mammals is mediated by the transcriptional cofactor GPS2 via direct mitochondria-to-nucleus translocation [ChIP-seq]

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