The plant-specific COST1 protein balances plant growth and drought tolerance via attenuation of autophagy
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA451423 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7056260.fastq.gz | Fastqsanger.gz | |||
| SRR7056270.fastq.gz | Fastqsanger.gz | |||
| SRR7056261.fastq.gz | Fastqsanger.gz | |||
| SRR7056271.fastq.gz | Fastqsanger.gz | |||
| SRR7056262.fastq.gz | Fastqsanger.gz |
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Project description:Plants balance their conflicting requirements for growth and stress tolerance via sophisticated pathways and unique genes that control responses to the external environment. We have identified a novel plant-specific gene, COST1(Constitutively Stressed 1), that affects plant growth and negatively regulates drought resistance by manipulating the autophagy pathway. An Arabidopsis cost1 mutant has decreased growth and increased drought tolerance, together with constitutive autophagy and increased expression of drought-response genes. The COST1 protein is degraded upon plant dehydration, and this degradation is blocked by treatment with inhibitors of the 26S proteasome or autophagy pathways. The cost1 mutant drought resistance is dependent on an active autophagy pathway, indicating that COST1 acts through manipulation of autophagy. COST1 co-localizes to autophagosomes with the autophagosome marker ATG8e and the autophagy adaptor NBR1, and physically interacts with ATG8e, indicating a pivotal role in direct regulation of autophagy. We propose a model in which COST1 represses autophagy under optimal conditions, thus allowing plant growth. During drought, COST1 is degraded, enabling activation of autophagy and suppressing growth to enhance drought tolerance.
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Project description:In plants, macroautophagy/autophagy has been reported to function in various biotic and abiotic stress-response pathways, but few direct regulators linking stress and autophagy have yet been identified. Other than the conserved nutrient sensing kinase TOR (Target of Rapamycin), negative regulators that can directly modulate plant autophagy are unknown. We recently identified a mutant, termed cost1 (Constitutively Stressed 1), which has strong drought tolerance with constitutive induction of autophagy and broad expression of normally stress-responsive genes. The COST1 protein negatively regulates autophagy by direct interaction with the key autophagy adaptor ATG8E, thus directly linking autophagy and drought tolerance. Moreover, plant growth and development in a cost1 mutant is greatly retarded, suggesting that COST1 controls the tradeoff between growth and stress tolerance.
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Project description:Plants balance their competing requirements for growth and stress tolerance via a sophisticated regulatory circuitry that controls responses to the external environments. We have identified a plant-specific gene, COST1 (constitutively stressed 1), that is required for normal plant growth but negatively regulates drought resistance by influencing the autophagy pathway. An Arabidopsis thaliana cost1 mutant has decreased growth and increased drought tolerance, together with constitutive autophagy and increased expression of drought-response genes, while overexpression of COST1 confers drought hypersensitivity and reduced autophagy. The COST1 protein is degraded upon plant dehydration, and this degradation is reduced upon treatment with inhibitors of the 26S proteasome or autophagy pathways. The drought resistance of a cost1 mutant is dependent on an active autophagy pathway, but independent of other known drought signaling pathways, indicating that COST1 acts through regulation of autophagy. In addition, COST1 colocalizes to autophagosomes with the autophagosome marker ATG8e and the autophagy adaptor NBR1, and affects the level of ATG8e protein through physical interaction with ATG8e, indicating a pivotal role in direct regulation of autophagy. We propose a model in which COST1 represses autophagy under optimal conditions, thus allowing plant growth. Under drought, COST1 is degraded, enabling activation of autophagy and suppression of growth to enhance drought tolerance. Our research places COST1 as an important regulator controlling the balance between growth and stress responses via the direct regulation of autophagy.
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