Abstract

Plants exposed to sulfur deficit elevate the transcription of NBR1 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.

Highlights

  • Autophagy is important for plant development, and plays a role in the response to various environmental stresses

  • We have previously reported that sulfur deficit increased the amount of Joka2 (NtNBR1) transcript encoding selective autophagy cargo receptor NBR1 in tobacco [7]

  • Concluding, our results suggest that NBR1 can fine-tune plant response to sulfur starvation

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Summary

Introduction

Autophagy is important for plant development, and plays a role in the response to various environmental stresses. One of the best characterized regulators of autophagy is the evolutionary conserved Target of Rapamycin (TOR) kinase that is on one hand activated by glucose and involved in the reciprocal regulation with plant hormones, and on the other hand, it stimulates such processes as translation, ribosome biogenesis, and cell proliferation (reviewed by [2,3]). In agreement with its overall growth promoting role, TOR kinase negatively regulates autophagy [4]. It is widely accepted that autophagy is a highly selective process targeting specific cargo (proteins, organelles) that must be removed at the particular growth condition or life stage. The selectivity of autophagy is ensured by the involvement of the selective autophagy cargo receptors

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