Screening and characterization of Chromobacterium piscinae AMA-5 for enhanced production of violacein and its ability of textile dyeing.

A violet pigment (violacein) bacterial isolate AMA-5 was isolated from soil samples collected from Achanakmar Biosphere Reserve, Mungeli district, Chhattisgarh, India. The yield of biocolor from this isolate was screened in minimal medium after 48 h of incubation at 37°C ± 2°C temperature. The violet pigment was extracted in ethanol. It was also observed that ammonium chloride (2.5 g/1000 mL) as a nitrogen source is the best to enhance AMA-5 pigment production among other nitrogen sources (ammonium sulfate, tryptophan, ammonium iron sulfate, and peptone). The Sanger sequencing of 16S rDNA of strain AMA-5 showed similarity with Chromobacterium piscinae. From the available literature and research articles, it was assumed that this violet color pigment is violacein. It was further verified by conducting high-performance liquid chromatography (HPLC), Fourier transform infrared spectroscopy (FTIR), and proton nuclear magnetic resonance (1H-NMR) analysis. The violet biocolor that extracted was used in cotton and polyester fabric dyeing. After the fabrics treated with sodium chloride as a mordant were completely dried, it was identified that the color was solidifying. Overall study showed that C. piscinae AMA-5 has good potential for production of violacein, which is the most important industrial natural dye used to add color to textile products.

Characterization of Arsenic-Resistant Klebsiella pneumoniae RnASA11 from Contaminated Soil and Water Samples and Its Bioremediation Potential.

Rapid industrialization and intensive agriculture activities have led to a rise in heavy metal contamination all over the world. Chhattisgarh (India) being an industrial state, the soil and water are thickly contaminated with heavy metals, especially from arsenic (As). In the present study, we isolated 108 arsenic-resistant bacteria (both from soil and water) from different arsenic-contaminated industrial and mining sites of Chhattisgarh to explore the bacterial gene pool. Further, we screened 24 potential isolates out of 108 for their ability to tolerate a high level of arsenic. The sequencing of the 16S rRNA gene of bacterial isolates revealed that all these samples belong to different diverse genera including Bacillus, Enterobacter, Klebsiella, Pantoea, Acinetobacter, Cronobacter, Pseudomonas and Agrobacterium. The metal tolerance ability was determined by amplification of arsB (arsenite efflux gene) and arsC (arsenate reductase gene) from chromosomal DNA of isolated RnASA11, which was identified as Klebsiella pneumoniae through in silico analysis. The bacterial strains RpSWA2 and RnASA11 were found to tolerate 600 mM As (V) and 30 mM As (III) but the growth of strain RpSWA2 was slower than RnASA11. Furthermore, atomic absorption spectroscopy (AAS) of the sample obtained from bioremediation assay revealed that Klebsiella pneumoniae RnASA11 was able to reduce the arsenic concentration significantly in the presence of arsenate (44%) and arsenite (38.8%) as compared to control.

Modulation of mitochondrial respiratory capacity by carrier-mediated transfer of RNA in vivo.

Genetic dysfunction of mitochondria is pathological, but an effective method of nucleic acid delivery to mitochondria in vivo is lacking. Injection into rodents of tagged polycistronic RNAs (pcRNAs) encoding parts of the organelle genome and bound to a carrier complex, resulted in rapid uptake and concentration of the RNA in many tissues. The delivered RNA was localized to mitochondria. A pan-genomic cocktail of pcRNAs restored mRNA levels, stimulated mitochondrial translation and respiratory capacity of skeletal muscle of middle-aged and old rats. Thus, the carrier-based protocol may be suitable for delivery of functional RNAs to mitochondria in vivo.

Mitochondrial gene therapy: The tortuous path from bench to bedside.

The association of mitochondrial dysfunction with a variety of human diseases and disabilities has been documented. Mitochondrial gene therapy (MGT) seeks to correct the genetic defect in mitochondrial DNA. For successful MGT, an appreciation of the nature of the dysfunction and of the complexities of mitochondrial disease is necessary. This review summarizes the current status of various MGT protocols described in the literature. Although there are many technical difficulties to be overcome, there are indications that some of them will find clinical applications in the near future.