TOR mediates the autophagy response to altered nucleotide homeostasis in an RNase mutant
TOR mediates the autophagy response to altered nucleotide homeostasis in an RNase mutant
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DOI：
10.1093/jxb/eraa410
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发表时间：
2020-12-31
影响因子：
6.9
通讯作者：
Bassham, Diane C.
中科院分区：
文献类型：
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作者：
Kazibwe, Zakayo;Soto-Burgos, Junmarie;Bassham, Diane C.
拟南芥T2家族核糖核酸内切酶RNS 2定位于液泡并在rRNA降解中起作用。RNS 2活性的丧失损害rRNA周转并导致组成性自噬，这是一种降解细胞组分的过程。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拯救rns 2 -2幼苗的组成性自噬表型，而嘌呤合成的抑制诱导野生型幼苗的自噬。rns 2 -2幼苗具有降低的雷帕霉素（TOR）激酶复合物（自噬的负调节物）的靶点活性，并且通过添加肌苷以增加嘌呤水平来挽救该表型。外源生长素激活rns 2 -2中的TOR阻断了增强的自噬，表明TOR信号通路可能参与了rns 2 -2突变体中自噬的激活。我们的数据表明了一种模型，其中rns 2 -2中rRNA降解的损失导致细胞质核苷酸浓度的降低，这反过来又抑制TOR活性，导致自噬激活以恢复稳态。
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.