Organic acid production and plant growth promotion as a function of phosphate solubilization by Acinetobacter rhizosphaerae strain BIHB 723 isolated from the cold deserts of the trans-Himalayas

An efficient phosphate-solubilizing plant growth–promoting Acinetobacter rhizosphaerae strain BIHB 723 exhibited significantly higher solubilization of tricalcium phosphate (TCP) than Udaipur rock phosphate (URP), Mussoorie rock phosphate (MRP) and North Carolina rock phosphate (NCRP). Qualitative and quantitative differences were discerned in the gluconic, oxalic, 2-keto gluconic, lactic, malic and formic acids during the solubilization of various inorganic phosphates by the strain. Gluconic acid was the main organic acid produced during phosphate solubilization. Formic acid production was restricted to TCP solubilization and oxalic acid production to the solubilization of MRP, URP and NCRP. A significant increase in plant height, shoot fresh weight, shoot dry weight, root length, root dry weight, and root, shoot and soil phosphorus (P) contents was recorded with the inoculated treatments over the uninoculated NP₀K or NP_TCPK treatments. Plant growth promotion as a function of phosphate solubilization suggested that the use of bacterial strain would be a beneficial addition to the agriculture practices in TCP-rich soils in reducing the application of phosphatic fertilizers.     

Degradation Kinetics of Caffeine and Related Methylxanthines by Induced Cells of <Emphasis Type="Italic">Pseudomonas</Emphasis> sp.

In this study, the kinetics of degradation of caffeine and related methylxanthines by induced cells of Pseudomonas sp. was performed. The kinetics data showed that degradation of caffeine, theobromine, and 7-methylxanthine followed Michealis–Menten kinetics. The values of K _m are low for caffeine and 7-methylxanthine and high for theobromine. Degradation of caffeine and theobromine was enhanced in the presence of NADH and NADPH, whereas the degradation of 7-methylxanthine was unaffected. Among the various metal ions tested, Fe²⁺ was found to enhance the rate of degradation for all three substrates, whereas Zn²⁺ and Cu²⁺ inhibited the degradation of caffeine and theobromine but not 7-methylxanthine. The differences in kinetic parameters and cofactor requirement suggest the possibility of the involvement of more than one N-demethylases in the caffeine catabolic pathway in Pseudomonas sp. The induced cells can serve as effective biocatalysts for the development of biodecaffeination techniques.     

TNF-induced activation of the Nox1 NADPH oxidase and its role in the induction of necrotic cell death

Tumor necrosis factor (TNF) is an important cytokine in immunity and inflammation and induces many cellular responses, including apoptosis and necrosis. TNF signaling enables the generation of superoxide in phagocytic and vascular cells through the activation of the NADPH oxidase Nox2/gp91. Here we show that TNF also activates the Nox1 NADPH oxidase in mouse fibroblasts when cells undergo necrosis. TNF treatment induces the formation of a signaling complex containing TRADD, RIP1, Nox1, and the small GTPase Rac1. TNF-treated RIP1-deficient fibroblasts fail to form such a complex, indicating that RIP1 is essential for Nox1 recruitment. Moreover, the prevention of TNF-induced superoxide generation with dominant-negative mutants of TRADD or Rac1, as well as knockdown of Nox1 using siRNA, inhibits necrosis. Thus our study suggests that activation of Nox1 through forming a complex with TNF signaling components plays a key role in TNF-induced necrotic cell death.     

Computational insights into diverse aspects of glutathione S-transferase gene family in Papaver somniferum

Journal of Plant Research - Plant glutathione S-transferases are an ancient protein superfamily having antioxidant activity. These proteins are primarily involved in diverse plant functions such as...     

Does mixed-species flocking influence how birds respond to a gradient of land-use intensity?

Conservation biology is increasingly concerned with preserving interactions among species such as mutualisms in landscapes facing anthropogenic change. We investigated how one kind of mutualism, mixed-species bird flocks, influences the way in which birds respond to different habitat types of varying land-use intensity. We use data from a well-replicated, large-scale study in Sri Lanka and the Western Ghats of India, in which flocks were observed inside forest reserves, in ‘buffer zones'' of degraded forest or timber plantations, and in areas of intensive agriculture. We find flocks affected the responses of birds in three ways: (i) species with high propensity to flock were more sensitive to land use; (ii) different flock types, dominated by different flock leaders, varied in their sensitivity to land use and because following species have distinct preferences for leaders, this can have a cascading effect on followers'' habitat selection; and (iii) those forest-interior species that remain outside of forests were found more inside flocks than would be expected by chance, as they may use flocks more in suboptimal habitat. We conclude that designing policies to protect flocks and their leading species may be an effective way to conserve multiple bird species in mixed forest and agricultural landscapes.     

Activation of Autophagic Flux against Xenoestrogen Bisphenol-A-induced Hippocampal Neurodegeneration via AMP kinase (AMPK)/Mammalian Target of Rapamycin (mTOR) Pathways

The human health hazards related to persisting use of bisphenol-A (BPA) are well documented. BPA-induced neurotoxicity occurs with the generation of oxidative stress, neurodegeneration, and cognitive dysfunctions. However, the cellular and molecular mechanism(s) of the effects of BPA on autophagy and association with oxidative stress and apoptosis are still elusive. We observed that BPA exposure during the early postnatal period enhanced the expression and the levels of autophagy genes/proteins. BPA treatment in the presence of bafilomycin A₁ increased the levels of LC3-II and SQSTM1 and also potentiated GFP-LC3 puncta index in GFP-LC3-transfected hippocampal neural stem cell-derived neurons. BPA-induced generation of reactive oxygen species and apoptosis were mitigated by a pharmacological activator of autophagy (rapamycin). Pharmacological (wortmannin and bafilomycin A₁) and genetic (beclin siRNA) inhibition of autophagy aggravated BPA neurotoxicity. Activation of autophagy against BPA resulted in intracellular energy sensor AMP kinase (AMPK) activation, increased phosphorylation of raptor and acetyl-CoA carboxylase, and decreased phosphorylation of ULK1 (Ser-757), and silencing of AMPK exacerbated BPA neurotoxicity. Conversely, BPA exposure down-regulated the mammalian target of rapamycin (mTOR) pathway by phosphorylation of raptor as a transient cell''s compensatory mechanism to preserve cellular energy pool. Moreover, silencing of mTOR enhanced autophagy, which further alleviated BPA-induced reactive oxygen species generation and apoptosis. BPA-mediated neurotoxicity also resulted in mitochondrial loss, bioenergetic deficits, and increased PARKIN mitochondrial translocation, suggesting enhanced mitophagy. These results suggest implication of autophagy against BPA-mediated neurodegeneration through involvement of AMPK and mTOR pathways. Hence, autophagy, which arbitrates cell survival and demise during stress conditions, requires further assessment to be established as a biomarker of xenoestrogen exposure.