Suitability of Brahmi (Bacopa monnieri L.) cultivation on fly ash-amended soil for better growth and oil content

Abstract

Sustainable application of fly ash and its management in agriculture is a major challenge nowadays. A pot culture experiment was conducted to find out the most suitable level of fly ash application for soil amendments that can improve the plant growth and productivity of Brahmi (Bacopa monnieri L.). After growing seedlings of B. monnieri under different levels of fly ash for 90?days, a significant increase in plant biomass, essential oil content and tolerance index (more than 100%) was observed under 25% of fly ash amended soil in comparison to garden soil and higher fly ash treatments. Leaf chlorophyll content and photosynthetic parameters were remained unchanged under 25% of fly ash as compared to seedlings grown on garden soil. However, these parameters were significantly declined under higher concentrations of fly ash treatments. Higher levels of fly ash caused oxidative damage and the induction of some antioxidative enzymes activities in B. monnieri indicates its capability to endure oxidative stress tolerance. Overall, our study showed that 25% of fly ash can be used as soil amendment for cultivation of B. monnieri L. leading to enhance plant biomass and essential oil production.     

Stimulation of K+ flux into mitochondria by phenylarsine oxide

The dithiol-reactive reagent phenylarsine oxide causes a pH-dependent stimulation of unidirectional K⁺ flux into respiring rat liver mitochondria. This stimulation is diminished by subsequent addition of either the dithiol 2,3-dimercaptopropanol or the monothiol 2-mercaptoethanol. In contrast, uncoupling by phenylarsine oxide is reversed by 2,3-dimercaptopropanol but not by 2-mercaptoethanol. The data suggest separate sites of interaction of phenylarsine oxide with mechanisms of K⁺ entry and ATP synthesis. Stimulatory effects of mersalyl and phenylarsine oxide on K⁺ influx are not additive. Thus PheASO and mersalyl may affect K⁺ influx at a common site. Pretreatment of the mitochondria with DCCD, which inhibits K⁺ influx, fails to alter sensitivity to PheAsO or mersalyl. Thus the DCCD binding site associated with the K⁺ influx mechanism appears to be separate from and independent of the sulfhydryl group(s) which mediate stimulation of K⁺ influx by PheAsO and mersalyl.PheAsO, like mersalyl, also increases the rate of unidirectional K⁺ efflux from respiring mitochondria. The combined presence of PheAsO plus mersalyl causes a greater stimulation of K⁺ efflux than is observed with either reagent alone.Abbreviations used: BAL, British AntilLewisite or 2,3-dimercaptopropanol; DCCD, dicyclohexylcarbodiimide; DBCT, dibutylchloromethyltin chloride; 2-ME, 2-mercaptoethanol; PheAsO, phenylarsine oxide.     

The effect of temperature on Agrobacterium tumefaciens-mediated gene transfer to plants

Agrobacterium tumefaciens is generally used to achieve genetic transformation of plants. The temperatures that have been used for infection with Agrobacterium in published transformation protocols differ widely and, to our knowledge, the effect of temperature on the efficiency of T-DNA transfer to plants has not been investigated systematically. Agrobacterium tumefaciens strains harbouring a binary vector with the β-glucuronidase ( uidA ) gene and either a nopaline-, an octopine- or an agropine/ succinamopine-type helper plasmid were tested in two transformation systems at temperatures between 15 and 29°C. One system involved cocultivation of Phaseolus acutifolius callus whereas in the other system Nicotiana tabacum leaves were vacuum-infiltrated. In both situations, irrespective of the type of helper plasmid, the levels of transient uidA expression decreased notably when the temperature was raised above 22°C. Expression was low at 27°C and undetectable at 29°C. We anticipate that the efficiency of many published transformation protocols can be improved by reconsidering the factor of temperature.     

Allantoin mediated regulation of miRNAs for short term salinity stress tolerance in Oryza sativa L. cv. IR-29

Journal of Plant Biochemistry and Biotechnology - Salinity affects plant in a variety of ways, including ion toxicity, osmotic stress and oxidative damage. Allantoin is a nitrogenous compound...     

Induction of the Serotonin1A Receptor in Neuronal Cells During Prolonged Stress and Degeneration

Abstract: Neuronal migration in brain is followed by differentiation of committed neurons and simultaneous apoptosis of uncommitted preneuronal cells due to a limiting supply of trophic factors and nutrients. We have dissected differentiation and apoptosis by designing a simple in vitro model for this nutrient deprivation using engineered neuronal cell lines stably transfected with a promoterless segment (G-21) of the intronless human serotonin_1A receptor (5-HT_1A-R) gene. Despite the use of widely different heterologous promoters (cytomegalovirus and Rous sarcoma virus) for the stable expression of G-21, a dramatic increase in expression of the 5-HT_1A-R (five- to 15-fold) and its mRNA was always observed during degeneration and apoptosis of nutrient-deprived neuronal cells. Involvement in this induction of a 170-bp 5'-end untranslated sequence (5'-UT) (tail end of the 500-bp natural promoter) of G-21 was confirmed by stable transfection of neuronal cells with an SV-40 promoter-driven construct harboring the 5'-UT and the reporter chloramphenicol acetyltransferase (CAT) cDNA. Presence of the 5'-UT resulted in a threefold increase in CAT expression during nutrient deprivation in randomly chosen clones. The induction was also observed in the endogenous 5-HT_1A-R, expressed by embryonic day 16 mouse hippocampal neurons, subsequent to nutrient deprivation and onset of degeneration. A trophic role of the 5-HT_1A-R has been suggested in earlier studies. Considering the example of protective heat shock proteins, which are induced during various types of stress, our results suggest that stressed neuronal cells undergoing degeneration and apoptosis synthesize increased levels of 5-HT_1A-R as a final attempt to survive.     

γ-Secretase Activity Is Required for Regulated Intramembrane Proteolysis of Tumor Necrosis Factor (TNF) Receptor 1 and TNF-mediated Pro-apoptotic Signaling

The γ-secretase protease and associated regulated intramembrane proteolysis play an important role in controlling receptor-mediated intracellular signaling events, which have a central role in Alzheimer disease, cancer progression, and immune surveillance. An increasing number of γ-secretase substrates have a role in cytokine signaling, including the IL-6 receptor, IL-1 receptor type I, and IL-1 receptor type II. In this study, we show that following TNF-converting enzyme-mediated ectodomain shedding of TNF type I receptor (TNFR1), the membrane-bound TNFR1 C-terminal fragment is subsequently cleaved by γ-secretase to generate a cytosolic TNFR1 intracellular domain. We also show that clathrin-mediated internalization of TNFR1 C-terminal fragment is a prerequisite for efficient γ-secretase cleavage of TNFR1. Furthermore, using in vitro and in vivo model systems, we show that in the absence of presenilin expression and γ-secretase activity, TNF-mediated JNK activation was prevented, assembly of the TNFR1 pro-apoptotic complex II was reduced, and TNF-induced apoptosis was inhibited. These observations demonstrate that TNFR1 is a γ-secretase substrate and suggest that γ-secretase cleavage of TNFR1 represents a new layer of regulation that links the presenilins and the γ-secretase protease to pro-inflammatory cytokine signaling.     

Elimination of Colon Cancer Stem-Like Cells by the Combination of Curcumin and FOLFOX

5-Fluorouracil (5-FU) or 5-FU plus oxaliplatin (FOLFOX) remains the backbone of colorectal cancer chemotherapeutics but with limited success. This could partly be due to the enrichment of cancer stem cells (CSCs) that are resistant to conventional chemotherapy. Therefore, validation of a nontoxic agent that can either cause reversal of chemoresistance or promote the killing of CSCs would be highly desirable. The current study examines whether curcumin, the major active ingredient of turmeric, either alone or together with FOLFOX, would be an effective strategy to eliminate colon CSCs. Exposure of colon cancer HCT-116 or HT-29 cells to FOLFOX that inhibited their growth led to the enrichment of CSC phenotype as evidenced by increased proportion of CD133-, CD44-, and/or CD166-positive cells and epidermal growth factor receptor (EGFR) levels. Treatment of FOLFOX-surviving colon cancer cells with either curcumin alone or together with FOLFOX resulted in a marked reduction in CSCs, as evidenced by the decreased expression of CD44 and CD166 as well as EGFR and by their ability to form anchorage-dependent colonies. They also caused disintegration of colonospheres. Increased expression of EGFR in FOLFOX-surviving cells could be attributed to hypomethylation of the EGFR promoter, whereas an opposite phenomenon was observed when the FOLFOX-surviving cells were treated with curcumin and/or FOLFOX. These changes were accompanied by parallel alterations in the levels of DNA methyltransferase 1. In conclusion, our data suggest that curcumin by itself or together with the conventional chemotherapeutic could be an effective treatment strategy for preventing the emergence of chemoresistant colon cancer cells by reducing/eliminating CSCs.