Abstract
The auxin receptor ABP1 directly regulates plasma membrane activities including the number of PIN-formed (PIN) proteins and auxin efflux transport. Red light (R) mediated by phytochromes regulates the steady-state level of ABP1 and auxin-inducible growth capacity in etiolated tissues but, until now, there has been no genetic proof that ABP1 and phytochrome regulation of elongation share a common mechanism for organ elongation. In far red (FR)-enriched light, hypocotyl lengths were larger in the abp1-5 and abp1/ABP1 mutants, but not in tir1-1, a null mutant of the TRANSPORT-INHIBITOR-RESPONSE1 auxin receptor. The polar auxin transport inhibitor naphthylphthalamic acid (NPA) decreased elongation in the low R:FR light-enriched white light (WL) condition more strongly than in the high red:FR light-enriched condition WL suggesting that auxin transport is an important condition for FR-induced elongation. The addition of NPA to hypocotyls grown in R- and FR-enriched light inhibited hypocotyl gravitropism to a greater extent in both abp1 mutants and in phyB-9 and phyA-211 than the wild-type hypocotyl, arguing for decreased phytochrome action in conjunction with auxin transport in abp1 mutants. Transcription of FR-enriched light-induced genes, including several genes regulated by auxin and shade, was reduced 3-5-fold in abp1-5 compared with Col and was very low in abp1/ABP1. In the phyB-9 mutant the expression of these reporter genes was 5–15-fold lower than in Col. In tir1-1 and the phyA-211 mutants shade-induced gene expression was greatly attenuated. Thus, ABP1 directly or indirectly participates in auxin and light signalling.
Highlights
Auxin initiates responses by at least two different receptors, AUXIN BINDING PROTEIN1 (ABP1) and TRANSPORT INHIBITOR RESPONSE1 (TIR1) (Scherer, 2011)
Heterozygous kanamycin-resistant abp1/ABP1 mutant seeds (Chen et al, 2001b) are in a Ws background and the genotypes verified as before (Chen et al, 2001b; Effendi et al, 2011). abp1-5 contains a mutation of a conserved histidine to a tyrosine (H94Y) (Robert et al, 2010) in the auxin-binding pocket of ABP1 (Woo et al, 2002). phyA-211 and phyB are in the Col-0 background and were obtained from M Zeidler,and tir1-1 and tir1-9 were obtained from M Quint
The gravitropic response of hypocotyls and the phototropic response to laterally applied blue light of hypocotyls of abp15, grown in the dark, was statistically indistinguishable from the wild type (Fig. 1a, c), the gravitropic response in roots was less than the wild type (Fig. 1b). abp1/ABP1 seedlings had an agravitropic and an aphototropic phenotype (Effendi et al, 2011)
Summary
Auxin initiates responses by at least two different receptors, AUXIN BINDING PROTEIN1 (ABP1) and TRANSPORT INHIBITOR RESPONSE1 (TIR1) (Scherer, 2011). ABP1-mediated rapid responses such as membrane hyperpolarization, channel regulation, proton extrusion, phospholipase A activation (Scherer and Andrè, 1989; Labusch et al, 2013), phospholipase D activation, transient increase in cytosolic calcium and elongation are too rapid to be reconciled with TIR1 as the only auxin receptor, assuming that the sole function of TIR1 is mediating changes in gene transcription through its degradation. Additional observations that active ABP1 is rate-limiting are: (i) the level of ABP1 and auxin-induced growth capacity is correlated in tobacco leaves (Chen et al, 2001b), (ii) genetic ablation of ABP1 blocks embryogenesis at an early phase when auxin induces the elongation of the top tier of cells (Chen et al, 2001b), and (iii) reduction of ABP1 reduces auxin-induced expansion without an effect on auxin-induced cell division (Jones et al, 1998)
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