Abstract
Vegetative growth requires the systemic coordination of numerous cellular processes, which are controlled by regulatory proteins that monitor extracellular and intracellular cues and translate them into growth decisions. In eukaryotes, one of the central factors regulating growth is the serine/threonine protein kinase Target of Rapamycin (TOR), which forms complexes with regulatory proteins. To understand the function of one such regulatory protein, Regulatory-Associated Protein of TOR 1B (RAPTOR1B), in plants, we analyzed the effect of raptor1b mutations on growth and physiology in Arabidopsis (Arabidopsis thaliana) by detailed phenotyping, metabolomic, lipidomic, and proteomic analyses. Mutation of RAPTOR1B resulted in a strong reduction of TOR kinase activity, leading to massive changes in central carbon and nitrogen metabolism, accumulation of excess starch, and induction of autophagy. These shifts led to a significant reduction of plant growth that occurred nonlinearly during developmental stage transitions. This phenotype was accompanied by changes in cell morphology and tissue anatomy. In contrast to previous studies in rice (Oryza sativa), we found that the Arabidopsis raptor1b mutation did not affect chloroplast development or photosynthetic electron transport efficiency; however, it resulted in decreased CO2 assimilation rate and increased stomatal conductance. The raptor1b mutants also had reduced abscisic acid levels. Surprisingly, abscisic acid feeding experiments resulted in partial complementation of the growth phenotypes, indicating the tight interaction between TOR function and hormone synthesis and signaling in plants.
Highlights
Vegetative growth requires the systemic coordination of numerous cellular processes, which are controlled by regulatory proteins that monitor extracellular and intracellular cues and translate them into growth decisions
Unlike in most eukaryotes, which have only one gene for this protein, RAPTOR is encoded by two homologous genes in the Arabidopsis genome (RAPTOR1A [AT5G01770] and RAPTOR1B [AT3G08850])
While the single KO of RAPTOR1A does not lead to visible phenotypes (Supplemental Fig. S1B), the double KO of RAPTOR1A and RAPTOR1B leads to arrested postembryonic growth and development (Anderson et al, 2005)
Summary
Vegetative growth requires the systemic coordination of numerous cellular processes, which are controlled by regulatory proteins that monitor extracellular and intracellular cues and translate them into growth decisions. Mutation of RAPTOR1B resulted in a strong reduction of TOR kinase activity, leading to massive changes in central carbon and nitrogen metabolism, accumulation of excess starch, and induction of autophagy These shifts led to a significant reduction of plant growth that occurred nonlinearly during developmental stage transitions. It turned out that only TORC1, which is composed of three core proteins, TOR, RAPTOR (Regulatory-Associated Protein of TOR), and LST8 (Lethal with Sec Thirteen8), was rapamycin sensitive; TORC2, which contains TOR, RICTOR (RapamycinInsensitive Companion of TOR), and LST8, was insensitive to the drug (Sarbassov et al, 2004) Based upon this essential difference, major progress in the understanding of the function and regulation of TORC1 was made in mammals and yeast (González and Hall, 2017; Saxton and Sabatini, 2017), while understanding of the rapamycin-insensitive TORC2 lagged behind. RAPTOR Controls Metabolic Balance regulator of anabolism, positively regulating all essential metabolic processes, including protein (Ma and Blenis, 2009), lipid (Lamming and Sabatini, 2013), and nucleotide metabolism (Ben-Sahra and Manning, 2017), while repressing catabolic processes like autophagy (Neufeld, 2010)
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
