Challenges to understand plant responses to wind

Understanding plant response to wind is complicated as this factor entails not only mechanical stress, but also affects leaf microclimate. In a recent study, we found that plant responses to mechanical stress (MS) may be different and even in the opposite direction to those of wind. MS-treated Plantago major plants produced thinner more elongated leaves while those in wind did the opposite. The latter can be associated with the drying effect of wind as is further supported by data on petiole anatomy presented here. These results indicate that plant responses to wind will depend on the extent of water stress. It should also be recognized that the responses to wind may differ between different parts of a plant and between plant species. Physiological research on wind responses should thus focus on the signal sensing and transduction of both the mechanical and drought signals associated with wind, and consider both plant size and architecture.Key words: biomechanics, leaf anatomy, phenotypic plasticity, plant architecture, signal transduction thigmomorphogenesis, windWind is one of the most ubiquitous environmental stresses, and can strongly affect development, growth and reproductive yield in terrestrial plants.^1–3 In spite of more than two centuries of research,⁴ plant responses to wind and their underlying mechanisms remain poorly understood. This is because plant responses to mechanical movement themselves are complicated and also because wind entails not only mechanical effects, but also changes in leaf gas and heat exchange.^5–7 Much research on wind has focused primarily on its mechanical effect. Notably, several studies that determine plant responses to mechanical treatments such as flexing, implicitly extrapolate their results to wind effects.^8–10 Our recent study¹¹ showed that this may lead to errors as responses to wind and mechanical stimuli (in our case brushing) can be different and even in the opposite direction. In this paper, we first separately discuss plant responses to mechanical stimuli, and other wind-associated effects, and then discuss future challenges for the understanding of plant responses to wind.It is often believed that responses to mechanical stress (thigmomorphogenesis) entail the production of thicker and stronger plant structures that resist larger forces. This may be true for continuous unidirectional forces such as gravity, however for variable external forces (such as wind loading or periodic flooding) avoiding such mechanical stress by flexible and easily reconfigurable structures can be an alternative strategy.^12–14 How plants adapt or acclimate to such variable external forces depends on the intensity and frequency of stress and also on plant structures. Reduced height growth is the most common response to mechanical stimuli.^15,16 This is partly because such short stature increases the ability of plants to both resist forces (e.g., real-locating biomass for radial growth rather than elongation growth), and because small plants experience smaller drag forces (Fig. 1). Some plant species show a resistance strategy in response to mechanical stress by increasing stem thickness^1,10 and tissue strength.⁷ But other species show an avoidance strategy by a reduction in stem or petiole thickness and flexural rigidity in response to MS.^11,15–18 These different strategies might be associated with plant size and structure. Stems of larger plants such as trees and tall herbs are restricted in the ability to bend as they carry heavy loads^7,10,19 (Fig. 1). Conversely short plants are less restricted in this respect and may also be prone to trampling for which stress-avoidance would be the only viable strategy.^18,20 Systematic understanding of these various responses to mechanical stress remains to be achieved.Open in a separate windowFigure 1A graphical representation of how wind effects can be considered to entail both a drying and a mechanical effect. Adaptation or acclimation to the latter can be through a force resistance strategy or a force avoidance strategy, the benefit of which may depend on the size and architecture of plants as well as the location of a given structure within a plant.Wind often enhances water stress by reducing leaf boundary layers and reduces plant temperature by transpiration cooling. The latter effect may be minor,¹¹ but the former could significantly affect plant development. Anten et al. (2010) compared phenotypic traits and growth of Plantago major that was grown under mechanical stimuli by brushing (MS) and wind in the factorial design. Both MS and wind treatments reduced growth and influenced allocation in a similar manner. MS plants, however, had more slender petioles and narrower leaf blades while wind exposed plants exhibited the opposite response having shorter and relatively thicker petioles and more round-shaped leaf blades. MS plants appeared to exhibit stress avoidance strategy while such responses could be compensated or overridden by water stress in wind exposure.¹¹ A further analysis of leaf petiole anatomy (Fig. 2) supports this view. The vascular fraction in the petiole cross-section was increased by wind but not by MS, suggesting that higher water transport was required under wind. Our results suggest that drying effect of wind can at least to some extent override its mechanical effect.Open in a separate windowFigure 2Representative images of petiole cross-sections of Plantago major grown in 45 days in continuous wind and/or mechanical stimuli (A–D). Petiole cross-section area (E) and vascular bundle fraction in the cross-section of petiole (F). mean + SD (n = 12) are shown. Significance levels of ANOVA; ***p < 0.001, **p < 0.01, *p < 0.05, ns p > 0.05.Physiological knowledge on plant mechanoreception and signal transduction has been greatly increased during the last decades. Plants sense mechanical stimuli through membrane strain with stretch activated channels²¹ and/or through some linker molecules connecting the cell wall, plasma membrane and cytoskeleton.^4,22,23 This leads to a ubiquitous increase in intracellular Ca²⁺ concentration. The increased Ca²⁺ concentration is sensed by touch induced genes (TCHs),^24,25 which activates downstream transduction machineries including a range of signaling molecules and phytohormones, consequently altering physiological and developmental processes.²⁶ Extending this knowledge to understand plant phenotypic responses to wind however remains a challenge. As responses to wind have been found to differ among parts of a plant (e.g., terminal vs. basal stem) and also across species, physiological studies should be extended to the whole-plant as integrated system rather than focusing on specific tissue level. Furthermore to understand the general mechanism across species, it is required to study different species from different environmental conditions. Advances in bioinformatics, molecular and physiological research will facilitate cross-disciplinary studies to disentangle the complicated responses of plants to wind.     

Changes in thylakoid membrane thickness associated with the reorganization of photosystem II light harvesting complexes during photoprotective energy dissipation

Using freeze-fracture electron microscopy we have recently shown that non-photochemical quenching (NPQ), a mechanism of photoprotective energy dissipation in higher plant chloroplasts, involves a reorganization of the pigment-protein complexes within the stacked grana thylakoids.¹ Photosystem II light harvesting complexes (LHCII) are reorganized in response to the amplitude of the light driven transmembrane proton gradient (ΔpH) leading to their dissociation from photosystem II reaction centers and their aggregation within the membrane.¹ This reorganization of the PSII-LHCII macrostructure was found to be enhanced by the formation of zeaxanthin and was associated with changes in the mobility of the pigment-protein complexes therein.¹ We suspected that the structural changes we observed were linked to the ΔpH-induced changes in thylakoid membrane thickness that were first observed by Murikami and Packer.^2,3 Here using thin-section electron microscopy we show that the changes in thylakoid membrane thickness do not correlate with ΔpH per se but rather the amplitude of NPQ and is thus affected by the de-epoxidation of the LHCII bound xanthophyll violaxanthin to zeaxanthin. We thus suggest that the change in thylakoid membrane thickness occurring during NPQ reflects the conformational change within LHCII proteins brought about by their protonation and aggregation within the membrane.Key words: nonphotochemical quenching, photoprotection, LHCII, photosystem II, thylakoid membrane     

Evidence for effect of random genetic drift on G+C content after lateral transfer of fucose pathway genes to Escherichia coli K-12

The cps cluster of Escherichia coli K-12 comprises genes involved in synthesis of capsular polysaccharide colanic acid. Part of the E. coli K-12 cps region has been cloned and sequenced and compared to its Salmonella enterica LT2 counterpart. The cps genes from the two organisms are homologous; in the case of the LT2 genes, with G+C content of 0.61 and codons characteristic of high G+C species, it seems clear that they have been acquired relatively recently by lateral transfer from a high G+C species. The K-12 form of these cps genes is closely related to those of LT2 so must derive from the same high G+C species, but it appears to have transferred much earlier such that random genetic drift has brought P3 (the corrected G+C content of codon base 3) down from 0.77 to 0.64, more than halfway to the E. coli average of 0.57. We estimate, using an equation developed by Sueoka, that the lateral transfer to E. coli took place approximately 45 million years ago. This is the first report we are aware of demonstrating the expected adjustment of P3 after lateral transfer between species with different G+C content DNA.      

Regulation of atrial natriuretic peptide release in normal humans.

Atrial volume, pressure, and heart rate are considered the most important modulators of atrial natriuretic peptide (ANP) release, although their relative role is unknown. Continuous positive-pressure breathing in normal humans may cause atrial pressure and atrial volume to go in opposite directions (increase and decrease, respectively). We utilized this maneuver to differentially manipulate atrial volume and atrial pressure and evaluate the effect on ANP release. Effective filling pressure (atrial pressure minus pericardial pressure) was also monitored, because this variable has been proposed as another modulator of ANP secretion. We measured right atrial (RA) pressure, RA area, esophageal pressure (reflection of pericardial pressure), and RA and peripheral venous ANP in seven healthy adult males at rest and during continuous positive-pressure breathing (19 mmHg for 15 min). Continuous positive-pressure breathing decreased RA area (mean +/- SE, *P less than 0.05) 13.6 +/- 1.1 to 10.5 +/- 0.8* cm2, increased RA pressure 4 +/- 1 to 16 +/- 1* mmHg, increased esophageal pressure 2 +/- 1 to 12 +/- 1* mmHg, and increased effective filling pressure 2 +/- 0 to 4 +/- 1* mmHg. RA ANP increased from 67 +/- 17 to 91 +/- 18* pmol/l and peripheral venous ANP from 43 +/- 4 to 58 +/- 6* pmol/l.(ABSTRACT TRUNCATED AT 250 WORDS)     

Detection of two loci involved in (1-->3)-beta-glucan (curdlan) biosynthesis by Agrobacterium sp. ATCC31749, and comparative sequence analysis of the putative curdlan synthase gene

Genes essential for the production of a linear, bacterial (1-->3)-beta- glucan, curdlan, have been cloned for the first time from Agrobacterium sp. ATCC31749. The genes occurred in two, nonoverlapping, genomic fragments that complemented different sets of curdlan( crd )-deficient transposon-insertion mutations. These were detected as colonies that failed to stain with aniline blue, a (1-->3)-beta-glucan specific dye. One fragment carried a biosynthetic gene cluster (locus I) containing the putative curdlan synthase gene, crdS, and at least two other crd genes. The second fragment may contain only a single crd gene (locus II). Determination of the DNA sequence adjacent to several locus I mutations revealed homology to known sequences only in the cases of crdS mutations. Complete sequencing of the 1623 bp crdS gene revealed highest similarities between the predicted CrdS protein (540 amino acids) and glycosyl transferases with repetitive action patterns. These include bacterial cellulose synthases (and their homologs), which form (1-->4)-beta-glucans. No similarity was detected with putative (1-->3)- beta-glucan synthases from yeasts and filamentous fungi. Whatever the determinants of the linkage specificity of these beta-glucan synthases might be, these results raise the possibility that (1-->3)-beta-glucans and (1-->4)-beta-glucans are formed by related catalytic polypeptides.      

Biochemical differentiation in bile duct cestodes and their marsupial hosts

Isozyme electrophoresis was used to assess possible cospeciation of parasites (cestodes of the Progamotaenia festiva complex) and their hosts (Australian diprotodont marsupials) and to compare the extent of interspecific genetic diversity of the parasites and their hosts. On the basis of morphology, there are three species in the complex, although electrophoresis revealed 14 distinct genetic types, most of which were host specific, although there were three cases of apparent host switching. The evolutionary relationships among the parasites were only partially concordant with those among the hosts. Moreover, the extent of electrophoretic diversity among the parasites was much higher than that among hosts.      

RhoA signaling modulates cyclin D1 expression in human lung fibroblasts; implications for idiopathic pulmonary fibrosis

Background

To elucidate further the pathogenesis of sporadic, idiopathic pulmonary arterial hypertension (IPAH) and identify potential therapeutic avenues, differential gene expression in IPAH was examined by suppression subtractive hybridisation (SSH).

Methods

Peripheral lung samples were obtained immediately after removal from patients undergoing lung transplant for IPAH without familial disease, and control tissues consisted of similarly sampled pieces of donor lungs not utilised during transplantation. Pools of lung mRNA from IPAH cases containing plexiform lesions and normal donor lungs were used to generate the tester and driver cDNA libraries, respectively. A subtracted IPAH cDNA library was made by SSH. Clones isolated from this subtracted library were examined for up regulated expression in IPAH using dot blot arrays of positive colony PCR products using both pooled cDNA libraries as probes. Clones verified as being upregulated were sequenced. For two genes the increase in expression was verified by northern blotting and data analysed using Student's unpaired two-tailed t-test.

Results

We present preliminary findings concerning candidate genes upregulated in IPAH. Twenty-seven upregulated genes were identified out of 192 clones examined. Upregulation in individual cases of IPAH was shown by northern blot for tissue inhibitor of metalloproteinase-3 and decorin (P < 0.01) compared with the housekeeping gene glyceraldehydes-3-phosphate dehydrogenase.

Conclusion

Four of the up regulated genes, magic roundabout, hevin, thrombomodulin and sucrose non-fermenting protein-related kinase-1 are expressed specifically by endothelial cells and one, muscleblind-1, by muscle cells, suggesting that they may be associated with plexiform lesions and hypertrophic arterial wall remodelling, respectively.     

Inclusion of low amounts of fructose with an intraportal glucose load increases net hepatic glucose uptake in the presence of relative insulin deficiency in dog

The effect of small amounts of fructose on net hepatic glucose uptake (NHGU) during hyperglycemia was examined in the presence of insulinopenia in conscious 42-h fasted dogs. During the study, somatostatin (0.8 microg.kg(-1).min(-1)) was given along with basal insulin (1.8 pmol.kg(-1).min(-1)) and glucagon (0.5 ng.kg(-1).min(-1)). After a control period, glucose (36.1 micromol.kg(-1).min(-1)) was continuously given intraportally for 4 h with (2.2 micromol.kg(-1).min(-1)) or without fructose. In the fructose group, the sinusoidal blood fructose level (nmol/ml) rose from <16 to 176 +/- 11. The infusion of glucose alone (the control group) elevated arterial blood glucose (micromol/ml) from 4.3 +/- 0.3 to 11.2 +/- 0.6 during the first 2 h after which it remained at 11.6 +/- 0.8. In the presence of fructose, glucose infusion elevated arterial blood glucose (micromol/ml) from 4.3 +/- 0.2 to 7.4 +/- 0.6 during the first 1 h after which it decreased to 6.1 +/- 0.4 by 180 min. With glucose infusion, net hepatic glucose balance (micromol.kg(-1).min(-1)) switched from output (8.9 +/- 1.7 and 13.3 +/- 2.8) to uptake (12.2 +/- 4.4 and 29.4 +/- 6.7) in the control and fructose groups, respectively. Average NHGU (micromol.kg(-1).min(-1)) and fractional glucose extraction (%) during last 3 h of the test period were higher in the fructose group (30.6 +/- 3.3 and 14.5 +/- 1.4) than in the control group (15.0 +/- 4.4 and 5.9 +/- 1.8). Glucose 6-phosphate and glycogen content (micromol glucose/g) in the liver and glucose incorporation into hepatic glycogen (micromol glucose/g) were higher in the fructose (218 +/- 2, 283 +/- 25, and 109 +/- 26, respectively) than in the control group (80 +/- 8, 220 +/- 31, and 41 +/- 5, respectively). In conclusion, small amounts of fructose can markedly reduce hyperglycemia during intraportal glucose infusion by increasing NHGU even when insulin secretion is compromised.