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Published on: July 29, 2019
TOR coordinates nucleotide availability with ribosome biogenesis in plants.
Michael Busche1,2, M Regina Scarpin1,2, Robert Hnasko3
1Department of Plant and Microbial Biology, University of California, Berkeley, CA 94720, USA.
Plant growth and metabolism are coordinated by TARGET OF RAPAMYCIN (TOR) signaling. This study identifies cytosolic phosphoribosyl pyrophosphate (PRPP) synthetase (PRS4) as essential for TOR activity, linking nucleotide synthesis to ribosome biogenesis and plant development.
Area of Science:
- Plant Biology
- Molecular Biology
- Biochemistry
Background:
- TARGET OF RAPAMYCIN (TOR) is a central regulator of cell growth and metabolism in eukaryotes, responding to nutrient availability.
- TOR signaling coordinates growth processes with cellular resources, but the precise mechanisms in plants are not fully elucidated.
Purpose of the Study:
- To identify essential genes that promote TOR activity in plants.
- To elucidate the role of nucleotide biosynthesis in TOR-mediated growth and ribosome biogenesis.
Main Methods:
- Medium-throughput functional genetic screen in Arabidopsis thaliana and Nicotiana benthamiana.
- Analysis of prs4 knockouts and knockdowns.
- Transcriptomic analysis (RNA-seq).
- Chemical and genetic inhibition of nucleotide biosynthesis pathways.
Main Results:
- Cytosolic phosphoribosyl pyrophosphate (PRPP) synthetase (PRS4) was identified as a critical regulator of TOR activity.
- prs4 mutants exhibit embryo-lethality, while PRS4 silencing causes developmental defects and repressed ribosome biogenesis.
- TOR activity is sensitive to nucleotide biosynthesis levels, with inhibition reversed by nucleobase supplementation.
- TOR promotes nucleotide biosynthesis to meet the demands of ribosomal RNA synthesis.
Conclusions:
- TOR signaling coordinates ribosome biogenesis with nucleotide availability in plants.
- This coordination is crucial for maintaining metabolic homeostasis and supporting overall plant growth.
- PRS4 is a key enzyme linking nutrient status to TOR-dependent growth regulation.
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