TOR mediates the autophagy response to altered nucleotide homeostasis in an RNase mutant. (9th September 2020)

• Record Type: Journal Article
• Authors: Kazibwe, Zakayo; Soto-Burgos, Junmarie; MacIntosh, Gustavo C; Bassham, Diane C
• Editors: Bozhkov, Peter
• Is Part Of: Journal of experimental botany. Volume 71:Number 22(2020)
• Page Start: 6907
• Page End: 6920
• Publication Date: 2020-09-09
• Subjects: Arabidopsis -- autophagy -- inosine -- nucleotides -- RNase -- RNS2 -- rRNA -- target of rapamycin (TOR); Botany -- Periodicals; Botany, Experimental -- Periodicals; Plant physiology -- Periodicals; 580
• DOI: 10.1093/jxb/eraa410
• Languages: English
• ISSNs: 0022-0957

Abstract

Abstract: The Arabidopsis thaliana T2 family endoribonuclease RNS2 localizes to the vacuole and functions in rRNA degradation. Loss of RNS2 activity impairs rRNA turnover and leads to constitutive autophagy, a process for degradation of cellular components. Autophagy is normally activated during environmental stress and is important for stress tolerance and homeostasis. Here we show that restoration of cytosolic purine nucleotide levels rescues the constitutive autophagy phenotype of rns2-2 seedlings, whereas inhibition of purine synthesis induces autophagy in wild-type seedlings. rns2-2 seedlings have reduced activity of the target of rapamycin (TOR) kinase complex, a negative regulator of autophagy, and this phenotype is rescued by addition of inosine to increase purine levels. Activation of TOR in rns2-2 by exogenous auxin blocks the enhanced autophagy, indicating a possible involvement of the TOR signaling pathway in the activation of autophagy in the rns2-2 mutant. Our data suggest a model in which loss of rRNA degradation in rns2-2 leads to a reduction in cytoplasmic nucleotide concentrations, which in turn inhibits TOR activity, leading to activation of autophagy to restore homeostasis. Abstract : Loss of the vacuolar RNase RNS2 causes the repression of TOR activity, possibly due to reduced cytosolic nucleotide concentrations, resulting in activation of autophagy.