Abstract
The perception and integration of stress stimuli with that of mitochondrion function are important during periods of perturbed cellular homeostasis. In a continuous effort to delineate these mitochondrial/stress-interacting networks, forward genetic screens using the mitochondrial stress response marker alternative oxidase 1a (AOX1a) provide a useful molecular tool to identify and characterize regulators of mitochondrial stress signaling (referred to as regulators of alternative oxidase 1a [RAOs] components). In this study, we reveal that mutations in genes coding for proteins associated with auxin transport and distribution resulted in a greater induction of AOX1a in terms of magnitude and longevity. Three independent mutants for polarized auxin transport, rao3/big, rao4/pin-formed1, and rao5/multidrug-resistance1/abcb19, as well as the Myb transcription factor rao6/asymmetric leaves1 (that displays altered auxin patterns) were identified and resulted in an acute sensitivity toward mitochondrial dysfunction. Induction of the AOX1a reporter system could be inhibited by the application of auxin analogs or reciprocally potentiated by blocking auxin transport. Promoter activation studies with AOX1a::GUS and DR5::GUS lines further confirmed a clear antagonistic relationship between the spatial distribution of mitochondrial stress and auxin response kinetics, respectively. Genome-wide transcriptome analyses revealed that mitochondrial stress stimuli, such as antimycin A, caused a transient suppression of auxin signaling and conversely, that auxin treatment repressed a part of the response to antimycin A treatment, including AOX1a induction. We conclude that mitochondrial stress signaling and auxin signaling are reciprocally regulated, balancing growth and stress response(s).
Highlights
The perception and integration of stress stimuli with that of mitochondrion function are important during periods of perturbed cellular homeostasis
A putative rao3 line exhibited increased expression of LUC under these conditions with 2.5-fold more abundant LUC protein after 6 h of chemical stimulation compared with seedlings from the control line Columbia-0 (Col):LUC containing the LUC gene driven by the alternative oxidase 1a (AOX1a) promoter and used for mutagenesis (Fig. 1, A and B; Ng et al, 2013a). (In this study, the Col:LUC line refers to the AOX1a:LUC construct [see above] in the Col ecotype and is used throughout as the internal control line in all experiments tested.) The rao3 line identified was further able to sustain these maximal levels to the end of the studied period (24 h; Fig. 1, A and B)
It was concluded that the signaling pathways that lead to the induction of AOX1a and auxin signaling are reciprocally regulated
Summary
The perception and integration of stress stimuli with that of mitochondrion function are important during periods of perturbed cellular homeostasis. PIN activity is regulated on a posttranslational level by constitutive vesicular cycling of PIN proteins between the endosomal compartment and the plasma membrane (PM), and both MDR1 (Noh et al, 2001) and Attenuated Shade Avoidance (ASA1)/BIG, a calossin-like protein, are required for PIN stabilization at the PM (Noh et al, 2001; Paciorek et al, 2005) Auxin itself inhibits this endocytosis and promotes its own efflux from cells (Paciorek et al, 2005). Several IAA structural analogs are induced on oxidative stress stimuli (e.g. oxindole 3-acetic acid; Peer et al, 2013), and indole 3-butyric acid (Tognetti et al, 2010) or basal defense responses activated during biotic stress (e.g. indole 3-carboxylic acid; Gamir et al, 2012), reducing available IAA levels Another mechanism to alter auxin homeostasis involves the subcellular distribution of IAA. Induction of AOX1a Is Antagonistic to Auxin Signaling as a result of auxin-dependent feedback mechanisms remain fragmentary
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