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A selective autophagy cargo receptor NBR1 modulates abscisic acid signalling in Arabidopsis thaliana.

Abstract：

:The plant selective autophagy cargo receptor neighbour of breast cancer 1 gene (NBR1) has been scarcely studied in the context of abiotic stress. We wanted to expand this knowledge by using Arabidopsis thaliana lines with constitutive ectopic overexpression of the AtNBR1 gene (OX lines) and the AtNBR1 Knock-Out (KO lines). Transcriptomic analysis of the shoots and roots of one representative OX line indicated differences in gene expression relative to the parental (WT) line. In shoots, many differentially expressed genes, either up- or down-regulated, were involved in responses to stimuli and stress. In roots the most significant difference was observed in a set of downregulated genes that is mainly related to translation and formation of ribonucleoprotein complexes. The link between AtNBR1 overexpression and abscisic acid (ABA) signalling was suggested by an interaction network analysis of these differentially expressed genes. Most hubs of this network were associated with ABA signalling. Although transcriptomic analysis suggested enhancement of ABA responses, ABA levels were unchanged in the OX shoots. Moreover, some of the phenotypes of the OX (delayed germination, increased number of closed stomata) and the KO lines (increased number of lateral root initiation sites) indicate that AtNBR1 is essential for fine-tuning of the ABA signalling pathway. The interaction of AtNBR1 with three regulatory proteins of ABA pathway (ABI3, ABI4 and ABI5) was observed in planta. It suggests that AtNBR1 might play role in maintaining the balance of ABA signalling by controlling their level and/or activity.

journal_name

Sci Rep

journal_title

Scientific reports

authors

Tarnowski L,Rodriguez MC,Brzywczy J,Piecho-Kabacik M,Krčkova Z,Martinec J,Wawrzynska A,Sirko A

doi

10.1038/s41598-020-64765-z

subject

Has Abstract

pub_date

2020-05-08 00:00:00

pages

7778

issue

1

issn

2045-2322

pii

10.1038/s41598-020-64765-z

journal_volume

10

pub_type

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