Hypocotyl Transcriptome Reveals Auxin Regulation of Growth-Promoting Genes through GA-Dependent and -Independent Pathways

Section of Cell and Developmental Biology, Division of Biological Sciences, University of California San Diego, La Jolla, California, United States of America.
PLoS ONE (Impact Factor: 3.23). 05/2012; 7(5):e36210. DOI: 10.1371/journal.pone.0036210
Source: PubMed


Many processes critical to plant growth and development are regulated by the hormone auxin. Auxin responses are initiated through activation of a transcriptional response mediated by the TIR1/AFB family of F-box protein auxin receptors as well as the AUX/IAA and ARF families of transcriptional regulators. However, there is little information on how auxin regulates a specific cellular response. To begin to address this question, we have focused on auxin regulation of cell expansion in the Arabidopsis hypocotyl. We show that auxin-mediated hypocotyl elongation is dependent upon the TIR1/AFB family of auxin receptors and degradation of AUX/IAA repressors. We also use microarray studies of elongating hypocotyls to show that a number of growth-associated processes are activated by auxin including gibberellin biosynthesis, cell wall reorganization and biogenesis, and others. Our studies indicate that GA biosynthesis is required for normal response to auxin in the hypocotyl but that the overall transcriptional auxin output consists of PIF-dependent and -independent genes. We propose that auxin acts independently from and interdependently with PIF and GA pathways to regulate expression of growth-associated genes in cell expansion.

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Available from: Cristina Castillejo, Jul 08, 2014
    • "Analysis of the hypocotyl epidermal cells showed that ACC rescues the hypocotyl-length phenotype under 2DIF by enhancing cell elongation (Fig. 2D). Because the action of ethylene is tightly linked to that of auxin (Muday et al., 2012) and auxin has also been linked to the regulation of cell elongation (Chapman et al., 2012; Nakayama et al., 2012), we subsequently investigated the role of auxin and its relation to ethylene in the seedling growth response to 2DIF. "
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    ABSTRACT: We demonstrate that antiphase light/temperature cycles (-DIF) inhibit hypocotyl growth in Arabidopsis (Arabidopsis thaliana). This is caused by reduced cell elongation during the cold photoperiod. Cell elongation in the basal part of the hypocotyl under -DIF was restored by both ACC (ethylene precursor) and auxin, indicating limited auxin and ethylene signaling under -DIF. Both auxin biosynthesis and auxin signaling were reduced during -DIF. In addition, expression of several ACC Synthases (ACS) was reduced under -DIF, but could be restored by auxin application. In contrast, the reduced hypocotyl elongation of ethylene biosynthesis and signaling mutants could not be complemented by auxin, indicating that auxin functions upstream of ethylene. The PHYTOCHROME INTERACTING FACTORS (PIF), PIF3, PIF4, and PIF5 were previously shown to be important regulators of hypocotyl elongation. We now demonstrate that, in contrast to pif4 and pif5 mutants, the reduced hypocotyl length in pif3 cannot be rescued by either ACC or auxin. In line with this, treatment with ethylene or auxin inhibitors reduced hypocotyl elongation in PIF4ox (overexpressor) and PIF5ox, but not in PIF3ox plants. PIF3 promoter activity was strongly reduced under -DIF but could be restored by auxin application in an ACS dependent manner. Combined these results show that PIF3 regulates hypocotyl length downstream, while PIF4/5 regulate hypocotyl length upstream of an auxin and ethylene cascade. We show that under -DIF lower auxin biosynthesis activity limits the signaling in this pathway, resulting in low activity of PIF3 and short hypocotyls. Copyright © 2014, American Society of Plant Biologists.
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    • "This is in contrast to the indeterminately growing PR, which has the capacity to determine new sites for LRP formation while it extends into the environment. The final length of the hypocotyl mainly depends on environmental factors such as light and hormones, including auxin, GA, and brassinosteroids (Jensen et al., 1998; Cowling and Harberd, 1999; De Grauwe et al., 2005; Vandenbussche et al., 2005; Chapman et al., 2012). "
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    • "Therefore, ARF6 appears to function mainly as a transcriptional activator, consistent with previous study (Tiwari et al., 2003). Comparison with auxin-activated genes (Chapman et al., 2012) identified 255 ARF6 binding targets that are activated by auxin in the hypocotyl tissues. These include many genes known to promote cell elongation (PREs, BIM1, BEE1 and HAT2, SAURs) and many genes with known function in auxin response, such as AUX/IAAs, PINs and PINOID (Figure 1— source data 2). "
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