Overexpression of the Selective Autophagy Cargo Receptor NBR1 Modifies Plant Response to Sulfur Deficit

Plants exposed to sulfur deficit elevate the transcription of <i>NBR1</i> 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...

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Main Authors: Leszek Tarnowski, Milagros Collados Rodriguez, Jerzy Brzywczy, Dominik Cysewski, Anna Wawrzynska, Agnieszka Sirko
Format: Article
Language:English
Published: MDPI AG 2020-03-01
Series:Cells
Subjects:
Online Access:https://www.mdpi.com/2073-4409/9/3/669
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author Leszek Tarnowski
Milagros Collados Rodriguez
Jerzy Brzywczy
Dominik Cysewski
Anna Wawrzynska
Agnieszka Sirko
author_facet Leszek Tarnowski
Milagros Collados Rodriguez
Jerzy Brzywczy
Dominik Cysewski
Anna Wawrzynska
Agnieszka Sirko
author_sort Leszek Tarnowski
collection DOAJ
description Plants exposed to sulfur deficit elevate the transcription of <i>NBR1</i> 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.
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spelling doaj.art-cdf88018bdd645d68ae1f3547a0481bb2023-09-02T12:00:25ZengMDPI AGCells2073-44092020-03-019366910.3390/cells9030669cells9030669Overexpression of the Selective Autophagy Cargo Receptor NBR1 Modifies Plant Response to Sulfur DeficitLeszek Tarnowski0Milagros Collados Rodriguez1Jerzy Brzywczy2Dominik Cysewski3Anna Wawrzynska4Agnieszka Sirko5Department of Plant Biochemistry, Institute of Biochemistry and Biophysics Polish Academy of Sciences, Pawińskiego 5A St, 02-106 Warsaw, PolandDepartment of Plant Biochemistry, Institute of Biochemistry and Biophysics Polish Academy of Sciences, Pawińskiego 5A St, 02-106 Warsaw, PolandDepartment of Plant Biochemistry, Institute of Biochemistry and Biophysics Polish Academy of Sciences, Pawińskiego 5A St, 02-106 Warsaw, PolandLaboratory of Mass Spectrometry, Institute of Biochemistry and Biophysics Polish Academy of Sciences, Pawińskiego 5A St, 02-106 Warsaw, PolandDepartment of Plant Biochemistry, Institute of Biochemistry and Biophysics Polish Academy of Sciences, Pawińskiego 5A St, 02-106 Warsaw, PolandDepartment of Plant Biochemistry, Institute of Biochemistry and Biophysics Polish Academy of Sciences, Pawińskiego 5A St, 02-106 Warsaw, PolandPlants exposed to sulfur deficit elevate the transcription of <i>NBR1</i> 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.https://www.mdpi.com/2073-4409/9/3/669autophagyprotein-protein interactionsulfur deficittranscriptome<i>arabidopsis thaliana</i>
spellingShingle Leszek Tarnowski
Milagros Collados Rodriguez
Jerzy Brzywczy
Dominik Cysewski
Anna Wawrzynska
Agnieszka Sirko
Overexpression of the Selective Autophagy Cargo Receptor NBR1 Modifies Plant Response to Sulfur Deficit
Cells
autophagy
protein-protein interaction
sulfur deficit
transcriptome
<i>arabidopsis thaliana</i>
title Overexpression of the Selective Autophagy Cargo Receptor NBR1 Modifies Plant Response to Sulfur Deficit
title_full Overexpression of the Selective Autophagy Cargo Receptor NBR1 Modifies Plant Response to Sulfur Deficit
title_fullStr Overexpression of the Selective Autophagy Cargo Receptor NBR1 Modifies Plant Response to Sulfur Deficit
title_full_unstemmed Overexpression of the Selective Autophagy Cargo Receptor NBR1 Modifies Plant Response to Sulfur Deficit
title_short Overexpression of the Selective Autophagy Cargo Receptor NBR1 Modifies Plant Response to Sulfur Deficit
title_sort overexpression of the selective autophagy cargo receptor nbr1 modifies plant response to sulfur deficit
topic autophagy
protein-protein interaction
sulfur deficit
transcriptome
<i>arabidopsis thaliana</i>
url https://www.mdpi.com/2073-4409/9/3/669
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