Phylogenetic diversity and biotechnological potentials of marine bacteria from continental slope of eastern Arabian Sea

Marine environments are substantially untapped source for the isolation of bacteria with the capacity to produce various extracellular hydrolytic enzymes, which have important ecological roles and promising biotechnological applications. Hydrolases constitute a class of enzymes widely distributed in nature from bacteria to higher eukaryotes. Marine microbial communities are highly diverse and have evolved during extended evolutionary processes of physiological adaptations under the influence of a variety of ecological conditions and selection pressures. A number of marine hydrolases have been described, including amylases, lipases and proteases, which are being used extensively for biotechnological applications. The present study was carried out to isolate marine bacteria from continental slope sediments of the eastern Arabian Sea and explore their biotechnological potential. Among the 119 isolates screened, producers of amylases (15%), caseinases (40%), cellulases (40%), gelatinases (60%), lipases (26%), ligninases (33%), phytase (11%) and Malachite Green dye degraders (16%) were detected. Phylogenetic analysis based on 16S rRNA gene sequencing showed that predominant marine sediment bacteria possessing more than four enzymatic activities belonged to the phyla Firmicutes and Proteobacteria, was assigned to the genera Bacillus, Planococcus, Staphylococcus, Chryseomicrobium, Exiguobacterium and Halomonas. Biodegradation of the dye Malachite Green using the liquid decolorization assay showed that both the individual cultures (Bacillus vietnamensis, Planococcus maritimus and Bacillus pumilus) and their consortium were able to decolorize more than 70% of dye within 24?h of incubation. This is the first report on diversity and extracellular hydrolytic enzymatic activities and bioremediation properties of bacteria from continental slope sediment of eastern Arabian Sea.     

Fostering sustainable land restoration through circular economy‐governed transitions

Soil and land are critical common pool resources offering a multitude of ecosystem services (ES) and presently affected by degradation and unplanned exploitation. The present article therefore attempts to elucidate the importance of circular economy in boosting land restoration and realization of several sustainable development goals through efficient waste recycling and clean energy production from degraded lands combined with policy restructuring for aligning circularity with restoration. Integrative policy frameworks targeting a “sustainable restoration economy” can help improve the cost feasibility of restoration projects through circularization of resource value chains besides enhancing social welfare and ecological vitality.     

Overexpression of a conserved HSP40 chaperone reduces toxicity of several neurodegenerative disease proteins

TDP-43 and FUS are DNA/RNA binding proteins associated with neuronal inclusions in amyotrophic lateral sclerosis (ALS) patients. Other neurodegenerative diseases are also characterized by neuronal protein aggregates, e.g. Huntington's disease, associated with polyglutamine (polyQ) expansions in the protein huntingtin. Here we discuss our recent paper establishing similarities between aggregates of TDP-43 that have short glutamine and asparagine (Q/N)-rich modules and are soluble in detergents, with those of polyQ and PIN4C that have large Q/N-rich domains and are detergent-insoluble. We also present new, similar data for FUS. Together, we show that like overexpression of polyQ or PIN4C, overexpression of FUS or TDP-43 causes inhibition of the ubiquitin proteasome system (UPS) and toxicity, both of which are mitigated by overexpression of the Hsp40 chaperone Sis1. Also, in all cases toxicity is enhanced by the [PIN⁺] prion. In addition, we show that the Sis1 mammalian homolog DNAJBI reduces toxicity arising from overexpressed FUS and TDP-43 respectively in human embryonic kidney cells and primary rodent neurons. The common properties of these proteins suggest that heterologous aggregates may enhance the toxicity of a variety of disease-related aggregating proteins, and further that chaperones and the UPS may be key therapeutic targets for diseases characterized by protein inclusions.     

Molecular modelling studies of kdr mutations in voltage gated sodium channel revealed significant conformational variations contributing to insecticide resistance

Voltage gated sodium channels (VGSC) of mosquito vectors are the primary targets of dichlorodiphenyltrichloroethane (DDT) and other synthetic pyrethroids used in public health programmes. The knockdown resistant (kdr) mutations in VGSC are associated with the insecticide resistance especially in Anophelines. The present study is aimed to emphasize and demarcate the impact of three kdr-mutations such as L1014S, L1014F and L1014H on insecticide resistance. The membrane model of sodium transport domain of VGSC (STD-VGSC) was constructed using de novo approach based on domain and trans-membrane predictions. The comparative molecular modelling studies of wild type and mutant models of STD-VGSC revealed that L1014F mutant was observed to be near native to the wild type model in all the respects, but, L1014S and L1014H mutations showed drastic variations in the energy levels, root mean square fluctuations (RMSF) that resulted in conformational variations. The predicted binding sites also showed variable cavity volumes and RMSF in L1014S and L1014H mutants. Further, DDT also found be bound in near native manner to wild type in L1014F mutant and with variable orientation and affinities in L1014S and L1014H mutants. The variations and fluctuations observed in mutant structures explained that each mutation has its specific impact on the conformation of VGSC and its binding with DDT. The study provides new insights into the structure–function-correlations of mutant STD-VGSC structures and demonstrates the role and effects of kdr mutations on insecticide resistance in mosquito vectors.     

Disappearing Scales in Carps: Re-Visiting Kirpichnikov's Model on the Genetics of Scale Pattern Formation

The body of most fishes is fully covered by scales that typically form tight, partially overlapping rows. While some of the genes controlling the formation and growth of fish scales have been studied, very little is known about the genetic mechanisms regulating scale pattern formation. Although the existence of two genes with two pairs of alleles (S&s and N&n) regulating scale coverage in cyprinids has been predicted by Kirpichnikov and colleagues nearly eighty years ago, their identity was unknown until recently. In 2009, the ‘S’ gene was found to be a paralog of fibroblast growth factor receptor 1, fgfr1a1, while the second gene called ‘N’ has not yet been identified. We re-visited the original model of Kirpichnikov that proposed four major scale pattern types and observed a high degree of variation within the so-called scattered phenotype due to which this group was divided into two sub-types: classical mirror and irregular. We also analyzed the survival rates of offspring groups and found a distinct difference between Asian and European crosses. Whereas nude × nude crosses involving at least one parent of Asian origin or hybrid with Asian parent(s) showed the 25% early lethality predicted by Kirpichnikov (due to the lethality of the NN genotype), those with two Hungarian nude parents did not. We further extended Kirpichnikov''s work by correlating changes in phenotype (scale-pattern) to the deformations of fins and losses of pharyngeal teeth. We observed phenotypic changes which were not restricted to nudes, as described by Kirpichnikov, but were also present in mirrors (and presumably in linears as well; not analyzed in detail here). We propose that the gradation of phenotypes observed within the scattered group is caused by a gradually decreasing level of signaling (a dose-dependent effect) probably due to a concerted action of multiple pathways involved in scale formation.     

Recurrent dynamics of rupture transitions of giant lipid vesicles at solid surfaces

Single giant unilamellar vesicles (GUVs) rupture spontaneously from their salt-laden suspension onto solid surfaces. At hydrophobic surfaces, the GUVs rupture via a recurrent, bouncing ball rhythm. During each contact, the GUVs, rendered tense by the substrate interactions, porate, and spread a molecularly transformed motif of a monomolecular layer on the hydrophobic surface from the point of contact in a symmetric manner. The competition from pore closure, however, limits the spreading and produces a daughter vesicle, which re-engages with the substrate. At solid hydrophilic surfaces, by contrast, GUVs rupture via a distinctly different recurrent burst-heal dynamics; during burst, single pores nucleate at the contact boundary of the adhering vesicles, facilitating asymmetric spreading and producing a “heart”-shaped membrane patch. During the healing phase, the competing pore closure produces a daughter vesicle. In both cases, the pattern of burst-reseal events repeats multiple times, splashing and spreading the vesicular fragments as bilayer patches at the solid surface in a pulsatory manner. These remarkable recurrent dynamics arise, not because of the elastic properties of the solid surface, but because the competition between membrane spreading and pore healing, prompted by the surface-energy-dependent adhesion, determine the course of the topological transition.