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Interdependent nutrient availability and steroid hormone signals facilitate root growth plasticity

ABSTRACT: Interdependent nutrient availability and steroid hormone signals facilitate root growth plasticity

PROVIDER: PRJNA470669 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7139980.fastq.gz	Fastqsanger.gz
	SRR7139981.fastq.gz	Fastqsanger.gz
	SRR7139982.fastq.gz	Fastqsanger.gz
	SRR7139983.fastq.gz	Fastqsanger.gz
	SRR7139984.fastq.gz	Fastqsanger.gz

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Interdependent nutrient availability and steroid hormone signals facilitate root growth plasticity

Project description:Plants acquire essential elements from inherently heterogeneous soils, in which phosphate and iron availabilities vary. Consequently, plants developed adaptive strategies to cope with low iron and low phosphate levels, including alternation between root growth enhancement and attenuation. How this adaptive response is achieved remains unclear. Here, we found that low iron accelerates the root growth of Arabidopsis thaliana by activating brassinosteroid signaling, whereas low-phosphate-induced high iron accumulation inhibited it. Altered hormone signaling intensity also modulated iron accumulation in the root elongation and differentiation zones, constituting a feedback response between brassinosteroid and iron. Surprisingly, the early effect of low iron levels on root growth required the brassinosteroid receptor but the hormone ligand was negligible. The brassinosteroid receptor inhibitor BKI1, the transcription factors BES1/BZR1 and the ferroxidase LPR1, stood at the base of this feedback loop. Hence, shared brassinosteroid and iron regulatory components link nutrient status to root morphology, thereby driving the adaptive response.

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Project description:Cancer cell metabolism is heavily influenced by microenvironmental factors, including nutrient availability. Therefore, knowledge of microenvironmental nutrient levels is essential to understand tumor metabolism. To measure the extracellular nutrient levels available to tumors, we developed a quantitative metabolomics method to measure the absolute concentrations of >118 metabolites in plasma and tumor interstitial fluid, the extracellular fluid that perfuses tumors. Comparison of nutrient levels in tumor interstitial fluid and plasma revealed that the nutrients available to tumors differ from those present in circulation. Further, by comparing interstitial fluid nutrient levels between autochthonous and transplant models of murine pancreatic and lung adenocarcinoma, we found that tumor type, anatomical location and animal diet affect local nutrient availability. These data provide a comprehensive characterization of the nutrients present in the tumor microenvironment of widely used models of lung and pancreatic cancer and identify factors that influence metabolite levels in tumors.

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Project description:Iron deficiency hampers photosynthesis and is associated with chlorosis. We recently showed that iron deficiency-induced chlorosis depends on phosphorus availability. How plants integrate these cues to control chlorophyll accumulation is unknown. Here, we show that iron limitation downregulates photosynthesis genes in a phosphorus-dependent manner. Using transcriptomics and genome-wide association analysis, we identify two genes, PHT4;4 encoding a chloroplastic ascorbate transporter and bZIP58, encoding a nuclear transcription factor, which prevent the downregulation of photosynthesis genes leading to the stay-green phenotype under iron-phosphorus deficiency. Joint limitation of these nutrients induces ascorbate accumulation by activating expression of an ascorbate biosynthesis gene, VTC4, which requires bZIP58. Furthermore, we demonstrate that chloroplastic ascorbate transport prevents the downregulation of photosynthesis genes under iron-phosphorus combined deficiency through modulation of ROS homeostasis. Our study uncovers a ROS-mediated chloroplastic retrograde signaling pathway to adapt photosynthesis to nutrient availability.

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