Abstract
The auxin and ethylene pathways cooperatively regulate a variety of developmental processes in plants. Growth responses to ethylene are largely dependent on auxin, the key regulator of plant morphogenesis. Auxin, in turn, is capable of inducing ethylene biosynthesis and signaling, making the interaction of these hormones reciprocal. Recent studies discovered a number of molecular events underlying auxin-ethylene crosstalk. In this review, we summarize the results of fine-scale and large-scale experiments on the interactions between the auxin and ethylene pathways in Arabidopsis. We integrate knowledge on molecular crosstalk events, their tissue specificity, and associated phenotypic responses to decipher the crosstalk mechanisms at a systems level. We also discuss the prospects of applying systems biology approaches to study the mechanisms of crosstalk between plant hormones.
Highlights
Auxin is a key regulator of plant development from cell growth and division to tissue specification and morphogenesis [1,2,3]
Auxin binding to nuclear TRANSPORT INHIBITOR RESPONSE 1 (TIR1) and AUXIN SIGNALING F-BOX (AFB) receptors promotes proteolytic cleavage of the AUXIN/INDOLE-3-ACETIC ACID (AUX/IAA) repressors, thereby depressing AUXIN RESPONSE FACTOR (ARF) family transcription factors, which trigger the transcriptional response to auxin
EIN2 C-terminal domain (EIN2-C) stabilizes EIN3 and EIN3-LIKE 1 (EIL1) transcription factors by translational repression of EIN3 BINDING F-BOX1 and 2 (EBF1 and EBF2) mRNA in cytosol [12], and facilitates EIN3 binding to the targets in the nucleus recruiting a histone binding protein EIN2 NUCLEAR ASSOCIATED PROTEIN 1 (ENAP1) [15,16]
Summary
Auxin (indole-3-acetic acid, IAA) is a key regulator of plant development from cell growth and division to tissue specification and morphogenesis [1,2,3]. The essential role of auxin in governing developmental processes requires the establishment and maintenance of auxin gradients in tissues. This is achieved through the coordination of auxin biosynthesis, conjugation, and transport. Auxin binding to nuclear TRANSPORT INHIBITOR RESPONSE 1 (TIR1) and AUXIN SIGNALING F-BOX (AFB) receptors promotes proteolytic cleavage of the AUXIN/INDOLE-3-ACETIC ACID (AUX/IAA) repressors, thereby depressing AUXIN RESPONSE FACTOR (ARF) family transcription factors, which trigger the transcriptional response to auxin. EIN3 and EIL1 trigger the genes encoding various transcription factors, including multiple representatives of the APETALA2/ETHYLENE RESPONSE FACTOR (AP2/ERF) family, and thereby activate a transcriptional cascade [17]
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