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Most plant growth and development processes are regulated in one way or another by auxin. The best-studied mechanism by which auxin exerts its regulatory effects is through the nuclear auxin pathway (NAP). In this pathway, Auxin Response Factors (ARFs) are the transcription factors that ultimately determine which genes become auxin regulated by binding to specific DNA sequences. ARFs have primarily been studied in Arabidopsis thaliana , but recent studies in other species have revealed family-wide DNA binding specificities for different ARFs and the minimal functional system of the NAP system, consisting of a duo of competing ARFs of the A and B classes. In this review, we provide an overview of key aspects of ARF DNA binding such as auxin response elements (TGTCNN) and tandem repeat motifs, and consider how structural biology and in vitro studies help us understand ARF DNA preferences. We also highlight some recent aspects related to the regulation of ARF levels inside a cell, which may alter the DNA binding profile of ARFs in different tissues. We finally emphasize the need to study minimal NAP systems to understand fundamental aspects of ARF function, the need to characterize algal ARFs to understand how ARFs evolved, how cutting-edge techniques can increase our understanding of ARFs, and which remaining questions can only be answered by structural biology. [ABSTRACT FROM AUTHOR]

Asymmetric auxin distribution is instrumental for the differential growth that causes organ bending on tropic stimuli and curvatures during plant development. Local differences in auxin concentrations are achieved mainly by polarized cellular distribution of PIN auxin transporters, but whether other mechanisms involving auxin homeostasis are also relevant for the formation of auxin gradients is not clear. Here we show that auxin methylation is required for asymmetric auxin distribution across the hypocotyl, particularly during its response to gravity. We found that loss-of-function mutants in Arabidopsis IAA CARBOXYL METHYLTRANSFERASE1 (IAMT1) prematurely unfold the apical hook, and that their hypocotyls are impaired in gravitropic reorientation. This defect is linked to an auxin-dependent increase in PIN gene expression, leading to an increased polar auxin transport and lack of asymmetric distribution of PIN3 in the iamt1 mutant. Gravitropic reorientation in the iamt1 mutant could be restored with either endodermis-specific expression of IAMT1 or partial inhibition of polar auxin transport, which also results in normal PIN gene expression levels. We propose that IAA methylation is necessary in gravity-sensing cells to restrict polar auxin transport within the range of auxin levels that allow for differential responses. [ABSTRACT FROM AUTHOR]

Summary: High temperature is a general stress factor that causes a decrease in crop yield. It has been shown that auxin application reduces the male sterility caused by exposure to higher temperatures. However, widespread application of a hormone with vast effects on plant physiology may be discouraged in many cases. Therefore, the generation of new plant varieties that locally enhance auxin in reproductive organs may represent an alternative strategy. We have explored the possibility of increasing indole‐3‐acetic acid (IAA) in ovaries by reducing IAA methyltransferase1 (IAMT1) activity in Arabidopsis thaliana. The iamt1 mutant showed increased auxin signalling in funiculi, which correlated with a higher growth rate of wild‐type pollen in contact with mutant ovaries and premature ovule fertilization. While the production of seeds per fruit was similar in the wild type and the mutant at 20 °C, exposure to 29 °C caused a more severe decrease in fertility in the wild type than in the mutant. Loss of IAMT1 activity was also associated with the production of more nodes after flowering and higher tolerance of the shoot apical meristem to higher temperatures. As a consequence, the productivity of the iamt1 mutant under higher temperatures was more than double of that of the wild type, with almost no apparent trade‐off. [ABSTRACT FROM AUTHOR]