Department of Plant Biochemistry, Institute of Biochemistry and Biophysics Polish Academy of Sciences, Pawińskiego 5A St, 02-106 Warsaw, Poland.
Laboratory of Mass Spectrometry, Institute of Biochemistry and Biophysics Polish Academy of Sciences, Pawińskiego 5A St, 02-106 Warsaw, Poland.
Cells. 2020 Mar 10;9(3):669. doi: 10.3390/cells9030669.
Plants exposed to sulfur deficit elevate the transcription of what might reflect an increased demand for NBR1 in such conditions. Therefore, we investigated the role of this selective autophagy cargo receptor in plant response to sulfur deficit (-S). Transcriptome analysis of the wild type and NBR1 overexpressing plants pointed out differences in gene expression in response to -S. Our attention focused particularly on the genes upregulated by -S in roots of both lines because of significant overrepresentation of cytoplasmic ribosomal gene family. Moreover, we noticed overrepresentation of the same family in the set of proteins co-purifying with NBR1 in -S. One of these ribosomal proteins, RPS6 was chosen for verification of its direct interaction with NBR1 and proven to bind outside the NBR1 ubiquitin binding domains. The biological significance of this novel interaction and the postulated role of NBR1 in ribosomes remodeling in response to starvation remain to be further investigated. Interestingly, NBR1 overexpressing seedlings have significantly shorter roots than wild type when grown in nutrient deficient conditions in the presence of TOR kinase inhibitors. This phenotype probably results from excessive autophagy induction by the additive effect of NBR1 overexpression, starvation, and TOR inhibition.
植物在硫缺乏时会提高可能反映出在这种条件下对 NBR1 需求增加的基因的转录水平。因此,我们研究了这种选择性自噬货物受体在植物对硫缺乏(-S)的反应中的作用。野生型和 NBR1 过表达植物的转录组分析指出,在 -S 响应中基因表达存在差异。我们特别关注两条线的根中由于细胞质核糖体基因家族的显著过表达而上调的基因,因为它们在两条线的根中由于细胞质核糖体基因家族的显著过表达而上调。此外,我们注意到在与 -S 中 NBR1 共纯化的蛋白质集中,同样的家族存在过表达。这些核糖体蛋白之一,RPS6 被选择用于验证其与 NBR1 的直接相互作用,并被证明结合在 NBR1 泛素结合结构域之外。这种新的相互作用的生物学意义以及假定的 NBR1 在饥饿响应中对核糖体重塑的作用仍有待进一步研究。有趣的是,当在用 TOR 激酶抑制剂在营养缺乏条件下生长时,NBR1 过表达的幼苗的根比野生型明显短。这种表型可能是由于 NBR1 过表达、饥饿和 TOR 抑制的附加作用导致自噬过度诱导。