The roles and interactions of ethylene with gibberellins in the far-red enriched light-mediated growth of <Emphasis Type="Italic">Solanum lycopersicum</Emphasis> seedlings

Wild type (WT) tomato seedlings responded to a low red to far-red (R/FR) ratio with increased stem elongation, similar leaflet area expansion and lower shoot ethylene levels. The levels of endogenous growth-active GA₁ and its immediate precursor GA₂₀ were decreased by low R/FR ratio, whereas the levels of GA₁ catabolite, GA₈, increased. To examine the interaction of ethylene with GAs in regulating tomato shoot growth under low R/FR ratio, transgenic (T) seedlings bearing Le-ACS2 and Le-ACS4 antisense mRNA were utilized. Low R/FR ratio increased stem elongation and decreased ethylene levels in T tomato shoots, as it did in WT shoots. However, T stems were significantly taller than the WT stems under low R/FR ratio. Leaflet areas were significantly larger for T, than WT seedlings under both R/FR ratios. Low R/FR ratio did not decrease endogenous levels of GA₁ and GA₂₀ in T shoots, but did increase GA₈ levels, which were higher than in WT shoots. These results, and hormone/inhibitor application studies, showed that in tomato shoots subjected to low R/FR ratio, GAs play a growth-promotive role in stem elongation, whereas ethylene is growth-inhibitory. Further, these results may imply that decreasing ethylene production under low R/FR ratio causes increases in stem elongation and GA levels.     

The discovery and SAR of indoline-3-carboxamides—A new series of 5-HT6 antagonists

Antagonists of the 5-HT₆ receptor have been shown to improve cognitive function in a wide range of animal models and as such may prove to be attractive agents for the symptomatic treatment of cognitive disorders such as Alzheimer’s disease (AD) and schizophrenia. We report herein the identification and SAR around N-(2-aminoalkyl)-1-(arylsulfonyl)indoline-3-carboxamides—a novel chemotype of 5-HT₆ antagonists.     

Hypoglycemia induced changes in cholinergic receptor expression in the cerebellum of diabetic rats

Glucose homeostasis in humans is an important factor for the functioning of nervous system. Hypoglycemia and hyperglycemia is found to be associated with central and peripheral nerve system dysfunction. Changes in acetylcholine receptors have been implicated in the pathophysiology of many major diseases of the central nervous system (CNS). In the present study we showed the effects of insulin induced hypoglycemia and streptozotocin induced diabetes on the cerebellar cholinergic receptors, GLUT3 and muscle cholinergic activity. Results showed enhanced binding parameters and gene expression of Muscarinic M1, M3 receptor subtypes in cerebellum of diabetic (D) and hypoglycemic group (D + IIH and C + IIH). α7nAchR gene expression showed a significant upregulation in diabetic group and showed further upregulated expression in both D + IIH and C + IIH group. AchE expression significantly upregulated in hypoglycemic and diabetic group. ChAT showed downregulation and GLUT3 expression showed a significant upregulation in D + IIH and C + IIH and diabetic group. AchE activity enhanced in the muscle of hypoglycemic and diabetic rats. Our studies demonstrated a functional disturbance in the neuronal glucose transporter GLUT3 in the cerebellum during insulin induced hypoglycemia in diabetic rats. Altered expression of muscarinic M1, M3 and α7nAchR and increased muscle AchE activity in hypoglycemic rats in cerebellum is suggested to cause cognitive and motor dysfunction. Hypoglycemia induced changes in ChAT and AchE gene expression is suggested to cause impaired acetycholine metabolism in the cerebellum. Cerebellar dysfunction is associated with seizure generation, motor deficits and memory impairment. The results shows that cerebellar cholinergic neurotransmission is impaired during hyperglycemia and hypoglycemia and the hypoglycemia is causing more prominent imbalance in cholinergic neurotransmission which is suggested to be a cause of cerebellar dysfunction associated with hypoglycemia.     

Spatial prediction of malaria prevalence in an endemic area of Bangladesh

Background

Malaria is a major public health burden in Southeastern Bangladesh, particularly in the Chittagong Hill Tracts region. Malaria is endemic in 13 districts of Bangladesh and the highest prevalence occurs in Khagrachari (15.47%).

Methods

A risk map was developed and geographic risk factors identified using a Bayesian approach. The Bayesian geostatistical model was developed from previously identified individual and environmental covariates (p < 0.2; age, different forest types, elevation and economic status) for malaria prevalence using WinBUGS 1.4. Spatial correlation was estimated within a Bayesian framework based on a geostatistical model. The infection status (positives and negatives) was modeled using a Bernoulli distribution. Maps of the posterior distributions of predicted prevalence were developed in geographic information system (GIS).

Results

Predicted high prevalence areas were located along the north-eastern areas, and central part of the study area. Low to moderate prevalence areas were predicted in the southwestern, southeastern and central regions. Individual age and nearness to fragmented forest were associated with malaria prevalence after adjusting the spatial auto-correlation.

Conclusion

A Bayesian analytical approach using multiple enabling technologies (geographic information systems, global positioning systems, and remote sensing) provide a strategy to characterize spatial heterogeneity in malaria risk at a fine scale. Even in the most hyper endemic region of Bangladesh there is substantial spatial heterogeneity in risk. Areas that are predicted to be at high risk, based on the environment but that have not been reached by surveys are identified.

     

Effects of a Severe Frost on Riparian Rainforest Restoration in the Australian Wet Tropics: Foliage Retention by Species and the Role of Forest Shelter

Restoration of ecological communities that can withstand future climate and land use changes requires information on species responses to various natural disturbances. Frost is an important disturbance that regulates plant species distributions, and although rare in tropical rainforest, it can occur in upland areas, especially where deforestation has occurred. We report the impacts of a severe frost that occurred in June and July 2007 on the Atherton Tablelands, Queensland, Australia and caused extensive damage to riparian restoration plots of upland rainforest species. We estimated proportion foliage retention to (1) compare impacts across 45 species; (2) examine the influence of plant height on frost effects; and (3) determine if plantings under shelterbelts of mature trees received less damage. Species exhibited different levels of foliage retention. Species that were particularly frost resistant included those from riparian habitats and a conifer. Some heavily impacted species are deciduous and may survive frost by shedding leaves; this warrants further investigation. Plant canopy height above ground level was only weakly correlated to foliage retention. Sheltered plants were much less damaged than unsheltered conspecifics, suggesting a useful way to mitigate frost impacts. These principles should help guide the development of resilient ecological communities in frost‐prone areas.     

Perspectives on the genetic architecture of divergence in body shape in sticklebacks

The body shape of fishes encompasses a number of morphological traits that are intrinsically linked to functional systems and affect various measures of performance, including swimming, feeding, and avoiding predators. Changes in shape can allow a species to exploit a new ecological niche and can lead to ecological speciation. Body shape results from the integration of morphological, behavioral and physiological traits. It has been well established that functional interdependency among traits plays a large role in constraining the evolution of shape, affecting both the speed and the repeated evolution of particular body shapes. However, it is less clear what role genetic or developmental constraints might play in biasing the rate or direction of the evolution of body shape. Here, we suggest that the threespine stickleback (Gasterosteus aculeatus) is a powerful model system in which to address the extent to which genetic or developmental constraints play a role in the evolution of body shape in fishes. We review the existing data that begins to address these issues in sticklebacks and provide suggestions for future areas of research that will be particularly fruitful for illuminating the mechanisms that contribute to the evolution of body shape in fishes.     

Systematic search for putative new domain families in Mycoplasma gallisepticum genome

Background

Stem cell factor (SCF) receptor c-Kit is recognized as a key signaling molecule, which transduces signals for the proliferation, differentiation and survival of stem cells. Binding of SCF to its receptor triggers transactivation, leading to the recruitment of kinases and phosphatases to the docking platforms of c-Kit catalytic domain. Tyrosine phosphatase-1 (Shp-1) deactivates/attenuates 'Kit' kinase activity. Whereas, Asp816Val mutation in the Kit activation loop transforms kinase domain to a constitutively activated state (switch off-to-on state), in a ligand-independent manner. This phenomenon completely abrogates negative regulation of Shp-1. To predict the possible molecular basis of interaction between c-Kit and Shp-1, we have performed an in silico protein-protein docking study between crystal structure of activated c-Kit (phosphorylated c-Kit) and full length crystal structure of Shp-2, a close structural counterpart of Shp-1.

Findings

Study revealed a stretch of conserved amino acids (Lys818 to Ser821) in the Kit activation domain, which makes decisive H-bonds with N-sh2 and phosphotyrosine binding pocket residues of the phosphatase. These H-bonds may impose an inhibitory steric hindrance to the catalytic domain of c-Kit, there by blocking further interaction of the activation loop molecules with incoming kinases. We have also predicted a phosphotyrosine binding pocket in SH2 domains of Shp-1, which is found to be predominantly closer to a catalytic groove like structure in c-Kit kinase domain.

Conclusions

This study predicts that crucial hydrogen bonding between N-sh2 domain of Shp-1 and Kit activation loop can modulate the negative regulation of c-Kit kinase by Shp-1. Thus, this finding is expected to play a significant role in designing suitable gain-of-function c-Kit mutants for inducing conditional proliferation of hematopoietic stem cells.