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Plant Physiology 145:1-2 (2007) © 2007 American Society of Plant Biologists On the InsideRespiratory Acclimation to Elevated CO2About 30% to 70% of the CO2 fixed by photosynthesis is released back to the atmosphere each year by plant respiration. Given the projected doubling of atmospheric CO2 in the not-too-distant future, there is a need for a better understanding of how tissue and whole-plant respiration rates are affected by elevated CO2. Previous studies have shown that elevated CO2 can affect respiratory gene expression, enzyme content, and mitochondrial number in the leaves of C3 plants. Do Crassulacean acid metabolism plants respond similarly? Gomez-Casanovas et al. (pp. 49–61) have investigated the effects of elevated CO2 on the respiration rates of cladodes of the cactus Opuntia ficus-indica, an invasive obligate Crassulacean acid metabolism species in Mediterranean climate regions. This species is known to exhibit enhanced growth when exposed to elevated levels of atmospheric CO2. During the 9 months of the study, the respiration rates, maximum activity of cytochrome c oxidase, and the number of mitochondria decreased in plants grown at elevated CO2 as compared to controls. Plants grown at elevated CO2 levels also showed reduced cytochrome pathway activity and increased electron flow through the alternative pathway. Surprisingly, despite the growth enhancement of Opuntia plants grown at high [CO2] and their decreased cytochrome pathway activities, ATP production was decreased. Thus, high [CO2] conditions led to increases in biomass, while reducing the respiratory machinery, activity, and ATP yields of the plants. Simultaneously, O2 consumption rates per unit of mitochondria were maintained. One possible solution to this puzzle is that the cladodes of Opuntia plants grown at elevated CO2 may have reduced energy costs in terms of tissue maintenance and growth, and hence, lower respiratory energy demands. Carbon Fixation in Diatoms Marine planktonic diatoms are responsible for up to 20% of primary production on earth. Diatoms achieve this, despite CO2-limiting conditions in the oceans, by using CO2-concentrating mechanisms to increase the CO2 concentration around Rubisco. By increasing the ratio of CO2 to O2 this diminishes the wasteful process of photorespiration. It was long thought, based on studies of the transport of inorganic carbon across cellular membranes, that diatoms utilize biophysical CO2-concentrating mechanisms. However, evidence has recently emerged of C4 photosynthesis, a biochemical CO2-concentrating mechanism in the marine diatom Thalassiosira weissflogii. The case for C4 photosynthesis has been further strengthened by the occurrence of relevant genes in recently sequenced marine phytoplankton genomes, including the diatom Thalassiosira pseudonana. The hypothetical mechanism of unicellular C4 photosynthesis is a compartmentalized carboxylation-decarboxylation cycle analogous to terrestrial C4 plants, albeit utilizing different intracellular compartments rather than different specialized cells. In the proposed model, phosphoenolpyruvate carboxylase functions as primary carboxylase in the cytoplasm, forming oxaloacetate (C4) from phosphoenolpyruvate (C3) and HCO3. C4 acids are then transported into the chloroplast and decarboxylated by phosphoenolpyruvate carboxykinase, releasing CO2 that is refixed by Rubisco. To complete the cycle, C3 acids are transported back to the cytoplasm. Roberts et al. (pp. 230–235) studied the pathways of photosynthetic carbon assimilation in two diatoms. In T. weissflogii both C3 and C4 compounds were major initial products, whereas T. pseudonana produced mainly C3 and C6 compounds. The data provide evidence of C3-C4 intermediate photosynthesis in T. weissflogii, but exclusively C3 photosynthesis in T. pseudonana. Contrary to the suggestions of other researchers, the authors found that the labeling patterns were the same for cells grown at near-ambient and low CO2 concentrations. This study suggests that the photosynthetic pathways of diatoms are diverse and may involve combined CO2-concentrating mechanisms. Furthermore, it emphasizes the requirement for metabolic and functional genetic and enzymic analyses before accepting the presence of C4-metabolic enzymes as evidence for C4 photosynthesis. Ion Fluxes and Anaerobic Metabolites Toxic levels of fermentation products can potentially accumulate in waterlogged soils owing to the increased anaerobic metabolism of plant roots and soil microbes under such conditions. The extent to which the accumulation of toxic metabolites is causally linked to observed deficiencies of macronutrients in waterlogged soils is not clear. Pang et al. (pp. 266–276) have employed a noninvasive microelectrode ion flux technique with excellent spatial and temporal resolution to quantify the K+, H+, and Ca2+ ion flux responses of barley (Hordeum vulgare) roots following short- and long-term exposures to secondary metabolites associated with anaerobic soils. Two barley cultivars differing in their waterlogging tolerance were studied. The authors demonstrate that secondary metabolites (monocarboxylic and phenolic acids) associated with waterlogged soil conditions adversely affect root nutrient uptake, and that the perturbation to root ionic homeostasis is much stronger in waterlogging-sensitive genotypes. Accordingly, the authors suggest that plant tolerance to these secondary metabolites might be a useful trait to consider in breeding programs. A Regulator of Calcium Release in Plants and Yeast Forward genetic studies in model legumes, such as Medicago truncatula and Lotus japonicus, have revealed genes that are required for both legume nodulation and Nod factor signaling. Among them, the DMI (DOESN'T MAKE INFECTIONS) genes play a very early role in Nod factor signaling. dmi1 mutants are affected in many responses to Nod factors and particularly in the Nod factor-induced Ca2+ spiking response. In wild types, within 1 to 2 min of Nod factor application, a transient increase in cytosolic free calcium ([Ca2+]cyt) is detectable in root hair cells. This Ca2+ transient has been shown to depend on Ca2+ influx through the plasma membrane and is localized to the root hair tip. Following this initial [Ca2+]cyt transient, repetitive nucleus-associated Ca2+ oscillations are observed in the cytosol. The facts that DMI1 is essential for Nod factor-induced Ca2+ spiking and localizes to the nuclear envelope around which the major Ca2+ changes occur made it a strong candidate for playing a direct role in the formation of Ca2+ spikes. Subsequent studies revealed, however, that DMI1 encodes not a Ca2+ channel but a membrane protein with striking similarities to the archaebacterial Ca2+-gated K+ channel MthK. The cytosolic C terminus of DMI1 contains a regulator of the conductance of K+ domain that in MthK acts as a Ca2+-regulated gating ring controlling the activity of the channel. Moreover, earlier analyses of dmi1 mutants demonstrated that DMI1 is not required for Mastoparan-induced Ca2+ spiking. Peiter et al. (pp. 192–203) have now extended the analysis of dmi1 mutant alleles to include more dramatic alterations to the protein. They show that dmi1-2, a nonnodulating mutant that lacks the entire C terminus (including the regulator of the conductance of K+ domain) but maintains the full channel domain, does inhibit Mastoporan-induced Ca2+ oscillations, and that it appears to act as a dominant-negative allele since it interferes in the ability of wild-type DMI1 to activate appropriate nodulation. To shed light on the function of DMI1, the authors used yeast (Saccharomyces cerevisiae) as a heterologous expression system. When expressed in yeast, DMI1 and dmi1-2, respectively, induced hypersensitivity and hypertolerance to high Li+ and Na+ concentrations. Moreover, both the full-length and the truncated protein altered a Li+-sensitive hexose-induced [Ca2+]cyt transient originating from internal stores. The data suggest that DMI1 has the capacity to regulate Ca2+ release channels in both yeast and plants. GA and Cryptochrome Cryptochromes mediate blue light-dependent photomorphogenic responses, such as inhibition of hypocotyl elongation. In Arabidopsis (Arabidopsis thaliana), CRYPTOCHROME1 (CRY1) and CRY2 mediate blue light inhibition of hypocotyl elongation. To investigate the mechanism underlying blue light-induced inhibition of hypocotyl elongation, Zhao et al. (pp. 106–118) analyzed a genetic suppressor, scc7-D (suppressors of cry1cry2), which suppressed the long-hypocotyl phenotype of the cry1cry2 mutant in a light-dependent but wavelength-independent manner. scc7-D is a gain-of-expression allele of the GA2ox8 gene encoding a GA-inactivating enzyme, GA 2-oxidase. Could blue light simply be acting by enhancing GA inactivation? The authors show that increased expression of a GA2ox gene caused hypersensitive or constitutive photomorphogenesis, depending on the relative levels of GA2ox overexpression. They further demonstrate that cryptochromes are required for the blue light induction of GA2ox1 expression and blue light suppression of expression of two genes involved in GA biosynthesis. Surprisingly, no significant change in the GA4 (the most active GA type in Arabidopsis) content was detected in the whole-shoot samples of the wild- type or cry1cry2 seedlings grown in the dark or continuous blue light. Conceivably, cryptochromes may regulate responsiveness of the cells or tissues to GA and/or trigger cell- or tissue-specific changes of the level of other bioactive GAs. A Mitogen-Activated Protein Kinase Involved in Programmed Cell Death during Self-Incompatibility Self-incompatibility (SI) in higher plants is an important mechanism to prevent inbreeding and involves the specific rejection of incompatible (self) pollen. SI in Papaver rhoeas involves interaction of pistil S-locus determinants (S proteins) with a pollen receptor. An incompatible (self) interaction triggers rapid, SI-specific increases in [Ca2+]cyt and triggers programmed cell death (PCD) involving a caspase-3-like activity, resulting in the specific destruction of self pollen. Experimental evidence, including gain-of-function studies, has demonstrated the involvement of mitogen-activated protein kinases (MAPKs) in activation of defense responses, resulting in PCD. Previous studies have implicated a MAPK, specifically p56, in the SI-induced signaling cascade in Papaver pollen, but is p56 involved in PCD too? Li et al. (pp. 236–245) demonstrate that SI rapidly reduces pollen viability and that the MAPK cascade inhibitor U0126, which prevents the SI-induced activation of the p56 in incompatible pollen, rescues incompatible pollen, while its negative analog, U0124, does not. This strongly implicates the involvement of a MAPK in SI-mediated loss of pollen viability and cell death. SI also stimulates a caspase-3-like activity and later DNA fragmentation. Both these markers of PCD are significantly reduced by pretreatment with U0126, implicating the involvement of a MAPK in signaling during early PCD. As p56 appears to be the only MAPK activated by SI, these studies suggest that p56 could be the MAPK involved in mediating SI-induced PCD.
Department of Natural Sciences, Mercy College, Dobbs Ferry, New York 10522 FOOTNOTES www.plantphysiol.org/cgi/doi/10.1104/pp.104.900236 Related articles in Plant Physiol.:
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