At high ambient temperature, plants display dramatic stem elongation in an adaptive response to heat. This response is mediated by elevated levels of the phytohormone auxin and requires auxin biosynthesis, signaling, and transport pathways. The mechanisms by which higher temperature results in greater auxin accumulation are unknown, however. A basic helix-loop-helix transcription factor, PHYTOCHROME-INTERACTING FACTOR 4 (PIF4), is also required for hypocotyl elongation in response to high temperature. PIF4 also acts redundantly with its homolog, PIF5, to regulate diurnal growth rhythms and elongation responses to the threat of vegetative shade. PIF4 activity is reportedly limited in part by binding to both the basic helix-loop-helix protein LONG HYPO-COTYL IN FAR RED 1 and the DELLA family of growth-repressing proteins. Despite the importance of PIF4 in integrating multiple environmental signals, the mechanisms by which PIF4 controls growth are unknown. Here we demonstrate that PIF4 regulates levels of auxin and the expression of key auxin biosynthesis genes at high temperature. We also identify a family of SMALL AUXIN UP RNA (SAUR) genes that are expressed at high temperature in a PIF4-dependent manner and promote elongation growth. Taken together, our results demonstrate direct molecular links among PIF4, auxin, and elongation growth at high temperature.indole-3-acetic acid | TRYPTOPHAN AMINOTRANSFERASE OF ARABIDOPSIS 1 | CYP79B2 T he hormone indole-3-acetic acid (IAA, or auxin) is fundamental to plant growth and development, controlling many key aspects of shoot and root growth (1). When plants are grown at elevated temperatures, IAA levels increase, resulting in increased hypocotyl elongation (2, 3). Although genetic studies in Arabidopsis have demonstrated that this growth response is dependent on auxin biosynthesis, signaling, and transport pathways, precisely how high temperature promotes an increase in auxin levels has not been established. There are multiple pathways for the de novo synthesis of IAA, the major naturally occurring plant auxin, which are often classified according to whether or not they require the precursor tryptophan (4). Although progress has been made in elucidating some of the enzymes involved in IAA biosynthesis, our understanding of these pathways and their regulation remains rudimentary.In addition to auxin, the basic helix-loop-helix transcription factor PHYTOCHROME-INTERACTING FACTOR 4 (PIF4) is also required for temperature-dependent hypocotyl elongation (5, 6). PIF4 has emerged as a key regulator of elongation in response to external signals, such as temperature and light, as well as internal signals, including gibberellin and the circadian clock (7-12). In the present work, we investigated potential mechanistic links between PIF4 and IAA in the control of temperatureinduced hypocotyl elongation. We found that PIF4 promotes IAA biosynthesis, possibly by activating the expression of key IAA biosynthetic genes in a temperature-dependent manner. Results and DiscussionGiven that s...

Root hairs facilitate a plant's ability to acquire soil anchorage and nutrients. Root hair growth is regulated by the plant hormone auxin and dependent on localized synthesis, secretion, and modification of the root hair tip cell wall. However, the exact cell wall regulators in root hairs controlled by auxin have yet to be determined. In this study, we describe the characterization of ERULUS (ERU), an auxin-induced Arabidopsis receptor-like kinase, whose expression is directly regulated by ARF7 and ARF19 transcription factors. ERU belongs to the Catharanthus roseus RECEPTOR-LIKE KINASE 1-LIKE (CrRLK1L) subfamily of putative cell wall sensor proteins. Imaging of a fluorescent fusion protein revealed that ERU is localized to the apical root hair plasma membrane. ERU regulates cell wall composition in root hairs and modulates pectin dynamics through negative control of pectin methylesterase (PME) activity. Mutant eru (-/-) root hairs accumulate de-esterified homogalacturonan and exhibit aberrant pectin Ca-binding site oscillations and increased PME activity. Up to 80% of the eru root hair phenotype is rescued by pharmacological supplementation with a PME-inhibiting catechin extract. ERU transcription is altered in specific cell wall-related root hair mutants, suggesting that it is a target for feedback regulation. Loss of ERU alters the phosphorylation status of FERONIA and H-ATPases 1/2, regulators of apoplastic pH. Furthermore, H-ATPases 1/2 and ERU are differentially phosphorylated in response to auxin. We conclude that ERULUS is a key auxin-controlled regulator of cell wall composition and pectin dynamics during root hair tip growth.

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