Kazibwe Zakayo, Soto-Burgos Junmarie, MacIntosh Gustavo C, Bassham Diane C
Department of Genetics, Development and Cell Biology, Iowa State University, Ames, IA, USA.
Roy J. Carver Department of Biochemistry, Biophysics and Molecular Biology, Iowa State University, Ames, IA, USA.
J Exp Bot. 2020 Dec 31;71(22):6907-6920. doi: 10.1093/jxb/eraa410.
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.
拟南芥T2家族核糖核酸酶RNS2定位于液泡并在rRNA降解中发挥作用。RNS2活性的丧失会损害rRNA周转并导致组成型自噬，这是一种细胞成分降解过程。自噬通常在环境胁迫期间被激活，并且对于胁迫耐受性和稳态很重要。在这里，我们表明细胞质嘌呤核苷酸水平的恢复挽救了rns2-2幼苗的组成型自噬表型，而嘌呤合成的抑制则在野生型幼苗中诱导自噬。rns2-2幼苗中雷帕霉素靶标（TOR）激酶复合物（一种自噬负调节因子）的活性降低，并且通过添加肌苷以增加嘌呤水平来挽救该表型。外源性生长素激活rns2-2中的TOR可阻断增强的自噬，表明TOR信号通路可能参与rns2-2突变体中自噬的激活。我们的数据提出了一个模型，其中rns2-2中rRNA降解的丧失导致细胞质核苷酸浓度降低，进而抑制TOR活性，导致自噬激活以恢复稳态。
