Plant Stress Tolerance Requires Auxin-Sensitive Aux/IAA Transcriptional Repressors

Abstract

Summary The Aux/IAA proteins are auxin-sensitive repressors that mediate diverse physiological and developmental processes in plants [1, 2]. There are 29 Aux/IAA genes in Arabidopsis that exhibit unique but partially overlapping patterns of expression [3] (Figure S1A). Although some studies have suggested that individual Aux/IAA genes have specialized function, genetic analyses of the family have been limited by the scarcity of loss-of-function phenotypes [4]. Further, with a few exceptions, our knowledge of the factors that regulate Aux/IAA expression is limited [1, 5]. We hypothesize that transcriptional control of Aux/IAA genes plays a central role in the establishment of the auxin-signaling pathways that regulate organogenesis, growth, and environmental response. Here we describe a screen for transcription factors (TFs) that regulate the Aux/IAA genes. We identify TFs from 38 families including 26 members of the DREB/CBF family. Several DREB/CBF TFs directly promote transcription of the IAA5 and IAA19 genes in response to abiotic stress. Recessive mutations in these IAA genes result in decreased tolerance to stress conditions demonstrating a role for auxin in abiotic stress. Our results demonstrate that stress pathways interact with the auxin gene regulatory network (GRN) through transcription of the Aux/IAA genes. We propose that the Aux/IAA genes function as hubs that integrate genetic and environmental information to achieve the appropriate developmental or physiological outcome.

Molecular framework for TIR1/AFB-Aux/IAA-dependent auxin sensing controlling adventitious rooting in Arabidopsis

“…ARF6 and ARF8 (but not ARF17) retain PB1 in their structure, which makes them targets of Aux/IAA repressor proteins. Because most previous genetic studies of Aux/IAA genes focused on characterization of gain-of-function mutants and there are only a few recent characterizations of KO mutants (23,25), we attempted to identify potential Aux/IAA partners involved in the control of AR initiation in the Arabidopsis hypocotyl. Nevertheless, likely because AR formation is a quantitative trait, we identified six iaa KO mutants showing an increased number of ARs.…”

“…To date, genetic investigations of Aux/IAA genes have been hampered by the lack of obvious phenotype in the loss-of-function mutants (22). Nevertheless, recent careful characterization of a few of the mutants identified more precise functions in primary or LR development for IAA3 or IAA8 (23,24) or in the response to environmental stresses for IAA3, IAA5, IAA6 and IAA19 (25,26).…”

Prediction of condition-specific regulatory maps inArabidopsisusing integrated genomic data

“…These two types were merged, which resulted in a total of 1,812,475 non-redundant interactions. We also compiled a list of published TF-target interactions generated by literature curation and ChIP-seq (Jin et al 2016), eY1H (Taylor-Teeples et al 2014Sparks et al 2016;Shani et al 2017), and other methods. All interactions were merged and duplicates were removed, which resulted in a set of 1,866,371 interactions.…”

“…Previous studies have also identified a considerable number of binding sites from data obtained in vivo related to different environmental perturbations in plants. For example, binding sites were screened to construct regulatory networks in response to far red light (Chen et al 2014b(Chen et al , 2014a, hormone (Fan et al 2014;Song et al 2016a;Shani et al 2017) and fungal infection (Liu et al 2015) in Arabidopsis thaliana. In contrast to expression data, binding site data present direct evidences of TF-target interactions.…”

TF2Network: predicting transcription factor regulators and gene regulatory networks in Arabidopsis using publicly available binding site information

“…These peaks were annotated to the closest gene in TAIR10 (35). The Y1H derived interactions were directly downloaded from the original publications (5)(6)(7)(45)(46)(47)(48). Protein-protein interaction data were retrieved from the studies listed in Table 3 and Gene Ontology (GO) annotations were downloaded from TAIR (35) on 9 May 2017.…”