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Plant Physiology 150:1-2 (2009) © 2009 American Society of Plant Biologists On the InsideAbscisic Acid Receptors? Recently, several putative receptors for the phytohormone abscisic acid (ABA) have been tentatively identified. These include the nuclear flowering time protein FCA, the plastid-associated magnesium (Mg)-chelatase H subunit (CHLH), and a protein originally identified as membrane-bound G-protein coupled receptor 2 (GCR2). The identification of multiple ABA receptors was expected, as both extracellular and intracellular ABA perception occurs. Recently, it was demonstrated that FCA does not bind ABA, and the article reporting FCA as an ABA receptor has been retracted. In this issue, two contributions challenge the legitimacy of two of the remaining proposed receptors. Müller and Hansson (pp. 157–166) have analyzed the effects of ABA on Mg chelatase-deficient barley (Hordeum vulgare). They conclude that CHLH does not qualify as an ABA receptor in contrast to the Arabidopsis (Arabidopsis thaliana) protein. They presently cannot explain the differences in ABA response between the barley and the Arabidopsis CHLHs. Risk et al. (pp. 6–11) present evidence that the putative extracellular ABA receptor, GCR2, does not bind ABA. The authors propose that the differences in the reports of ABA binding are probably due to the variable quality of the purified proteins used. They propose that an improved method for measuring ABA binding is required and that the search for ABA receptors should continue. The putative Arabidopsis ABA receptors were all identified based on sequence analysis and bioinformatics approaches rather than by using direct biochemical or genetic approaches. It would seem, therefore, that more rigorous analyses of ABA binding are required when receptors have been identified based on a candidate gene approach. This necessity is reinforced in a letter by Jones and Sussman (pp. 3–5) wherein they propose that a plant protein, whether or not it shares sequence and/or predicted structure similarity to any known class of receptors, must meet strict biochemical criteria for receptor functionality before it is accepted as such.
The shoot apical meristem (SAM) initiates lateral organs and determines their regular geometric arrangement, or phyllotaxy. Although phyllotactic patterns have long drawn the attention of biologists and mathematicians, until recently the molecular mechanism underlying the generation of these patterns has been elusive. Recent developmental studies have supported a model in which the regulation of phyllotaxy is based on the polar transport of auxin by the PINFORMED1 (PIN1) auxin efflux carrier. Inhibition of polar auxin transport or mutations in the PIN1 auxin efflux carrier have been shown to disrupt leaf or flower initiation in several species. However, despite the strong implication of auxin in phyllotaxy regulation, no auxin mutants in Arabidopsis display obvious changes in their phyllotactic pattern. One of the very few mutants known to specifically affect phyllotaxy has been mapped to the ABERRANT PHYLLOTAXY1 (ABPH1) locus in maize (Zea mays). abph1 mutants develop a decussate phyllotaxy, in which leaves are paired at 180°; in contrast, normal maize plants exhibit a distichous phyllotaxy in which leaves develop in an alternate pattern. ABPH1 encodes a cytokinin-inducible type A response regulator, suggesting that cytokinin signals are important for phyllotaxy regulation in maize. In this issue, Lee et al. (pp. 42–54) further investigate the interaction between auxin and cytokinin signaling in maize phyllotaxy. They report that treatment with the polar auxin transport inhibitor 1-naphthylphthalamic acid greatly reduced the expression of ABPH1, suggesting that ABPH1 expression is dependent on accumulation of auxin at incipient leaf primordia. Their results indicate distinct roles for ABPH1 as a negative regulator of SAM size and a positive regulator of PIN1 expression. More specifically, the authors propose that reductions in auxin levels and PIN1 expression in the SAMs of abph1 mutants delay leaf initiation, thereby contributing to the enlarged SAM and altered phyllotaxy of these mutants. Thus, cross talk between auxin and cytokinin signaling appears to be important in determining phyllotaxy.
Cadmium (Cd) is a toxic element whose presence in the environment stems mainly from industrial processes and phosphate fertilizers. Cd inhibits seed germination, decreases plant growth and photosynthesis, and impairs the distribution of nutrients. Overall, the symptoms of chronic exposure to sublethal amounts of Cd mimic senescence. Two articles in this issue concern the signaling events controlling Cd cytotoxicity in plants. In the first case, De Michele et al. (pp. 217–228) show that Arabidopsis cell suspension cultures undergo a process of programmed cell death when exposed to Cd, and that this process resembled an accelerated senescence, as suggested by the expression of the senescence marker gene SAG12. Cd treatment was accompanied by a rapid increase in nitric oxide (NO) and phytochelatin synthesis, which continued to be high as long as cells remained viable. Hydrogen peroxide production was a later event and preceded the rise of cell death by about 24 h. The pharmacological inhibition of NO synthesis resulted in the partial prevention of hydrogen peroxide increase, SAG12 expression, and mortality, indicating that NO is required for Cd-induced cell death. In the second contribution, Rodríguez-Serrano et al. (pp. 229–243) used confocal laser microscopy to measure in vivo increases in NO and reactive oxygen species (ROS) production under conditions of Cd stress in pea (Pisum sativum) plants. Because NO synthase-derived NO production is dependent on calcium (Ca), the effect of this metal on NO and ROS production was also investigated. They report that a decrease in antioxidative superoxide dismutase activity was attributable to a Ca deficiency induced by Cd. Consistent with this finding, the application of exogenous Ca prevented the Cd-induced increase in ROS production. NO synthase-dependent NO production, on the other hand, was strongly depressed by Cd and treatment with Ca prevented this effect. The seemingly discordant results of these two articles in regard to the effects of Cd on NO production may be due to differences in the species examined, the experimental conditions employed, or the timing of events during Cd cytotoxicity.
Phospholipase D (PLD) catalyzes the hydrolysis of structural phospholipids to give phosphatidic acid (PA). In recent years, PLDs have been suggested to be involved in many plant cellular processes, including the signal transduction pathways induced by certain stresses and hormones. PA, which can be generated directly by the action of PLD, is an important lipid messenger that mediates the generation of ROS and activates wound-activated enzymes. Two contributions in this issue indicate that PLD may play complex and possibly contrary roles in plant defense. In the first contribution, Yamaguchi et al. (pp. 308–319) surveyed the genome of rice (Oryza sativa) and identified three PLD genes that were highly expressed in most tissues. To examine the physiological function of these PLDs in rice, the authors made knockdown plants for each of the highly expressed PLD isoforms by introducing gene-specific RNA interference constructs. One of these, namely, the OsPLDβ1-knockdown plant, accumulated ROS in the absence of pathogen infection. Reverse transcription-PCR and DNA microarray analyses revealed that the knockdown of OsPLDβ1 affected the regulation of more than 1,400 genes, including the induction of many defense-related genes. These results indicate that the OsPLDβ1-knockdown plants spontaneously activate defense responses in the absence of pathogen infection. Furthermore, the knockdown transgenic plant showed a marked increase in the disease resistance to the blast fungus, Pyricularia grisea, and the bacterial blight, Xanthomonas oryzae. These results clearly indicate that OsPLDβ1 functions as a negative regulator of defense responses and is involved in disease resistance in rice. Salicylic acid (SA) is another central player in defense responses against pathogen attack. SA accumulates in infected cells after pathogen recognition. In addition to this local accumulation, elevated levels of SA in plant tissues distal from the site of infection induce systemic acquired resistance against a broad range of pathogens. In this issue, Krinke et al. (pp. 424–436) investigated the involvement of PLD in SA signal transduction. A unique property of PLDs is their ability to use primary alcohols as an acceptor of a phosphatidyl moiety instead of a water molecule. Thus, in the presence of a primary alcohol, PLD catalyzes a transphosphatidylation reaction that leads to the formation of phosphatidylalcohol instead of PA. Secondary and tertiary alcohols are not substrates of the transphosphatidylation reaction. The authors show that the incubation of Arabidopsis cell suspensions with primary alcohols inhibited the induction of two SA-responsive genes, PR1 and WRKY38. Secondary or tertiary alcohols had no inhibitory effect. Thus, the SA-triggered n-butanol-sensitive pathway is likely to be a PLD-dependent pathway.
Carbon dioxide (CO2) is one of the most important greenhouse gases contributing to global warming. Increases in CO2 concentration will likely have a profound impact on plant growth. Previous studies have shown that elevated CO2 increases net photosynthesis rate in C3 plants because higher CO2 suppresses RuBP oxygenase activity, decreases photorespiration, and increases carbon assimilates for plant growth and development. As a consequence, elevated CO2 treatments generally increase the biomass of C3 plants. The enhancement of plant growth by elevated CO2 will also increase their demand for nutrients. Iron (Fe) is an essential micronutrient for plant growth and development. Although the total Fe content in soils regularly exceeds plant requirements, its bioavailability to plants is often limited, particularly in calcareous soils. Jin et al. (pp. 272–280) report that when tomato (Solanum lycopersicum) plants were grown in Fe-limited media and elevated CO2, their biomass and root-to-shoot ratio were greater than plants grown in ambient CO2. Furthermore, the associated increase in Fe concentrations in the shoots and roots alleviated Fe-deficiency-induced chlorosis. Elevated CO2 also increased the NO levels in roots. These results implicate an involvement of NO in enhancing Fe-deficiency-induced responses when Fe limitation and elevated CO2 occur together. The authors propose that the combination of elevated CO2 and Fe limitation induces morphological, physiological, and molecular responses that enhance the capacity of plants to access and utilize Fe from sparingly soluble sources such as Fe(III) oxide.
Division of Health Professions and Natural Sciences FOOTNOTES www.plantphysiol.org/cgi/doi/10.1104/pp.109.900291 Related articles in Plant Physiol.:
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