Heavy metals are natural constituents of the environment, but indiscriminate use for human purposes has altered their geochemical cycles and biochemical balance. This results in excess release of heavy metals such as cadmium, copper, lead, nickel, zinc etc. into natural resources like the soil and aquatic environments. Prolonged exposure and higher accumulation of such heavy metals can have deleterious health effects on human life and aquatic biota. The role of microorganisms and plants in biotransformation of heavy metals into nontoxic forms is well-documented, and understanding the molecular mechanism of metal accumulation has numerous biotechnological implications for bioremediation of OPEN ACCESSSustainability 2015, 7 2190 metal-contaminated sites. In view of this, the present review investigates the abilities of microorganisms and plants in terms of tolerance and degradation of heavy metals. Also, advances in bioremediation technologies and strategies to explore these immense and valuable biological resources for bioremediation are discussed. An assessment of the current status of technology deployment and suggestions for future bioremediation research has also been included. Finally, there is a discussion of the genetic and molecular basis of metal tolerance in microbes, with special reference to the genomics of heavy metal accumulator plants and the identification of functional genes involved in tolerance and detoxification.

In this review, a comprehensive discussion exclusively on bacterial xylanases; their gene organization; different factors and conditions affecting enzyme yield and activity; and their commercial application have been deliberated in the light of recent research findings and extensive information mining. Improved understanding of biological properties and genetics of bacterial xylanase will enable exploitation of these enzymes for many more ingenious biotechnological and industrial applications.

DNA methylation inhibitors such as 5-aza-2′-deoxycytidine (5-Aza-CdR) are currently used for the treatment of myelodysplastic syndrome. Although global DNA demethylation has been observed after treatment, it is unclear to what extent demethylation induces changes in nucleosome occupancy, a key determinant of gene expression. We use the colorectal cancer cell line HCT116 as a model to address this question and determine that <2% of regions demethylated by 5-Aza-CdR treatment assume an open configuration. Consolidating our findings, we detect nucleosome retention at sites of global DNA methylation loss in DKO1, an HCT116-derived non-tumorigenic cell-line engineered for DNA methyltransferase disruption. Notably, regions that are open in both HCT116 cells after treatment and in DKO1 cells include promoters belonging to tumor suppressors and genes under-expressed in colorectal cancers. Our results indicate that only a minority of demethylated promoters are associated with nucleosome remodeling, and these could potentially be the epigenetic drivers causing the loss of tumorigenicity. Furthermore, we show that the chromatin opening induced by the histone deacetylase inhibitor suberoylanilide hydroxamic acid has strikingly distinct targets compared with those of 5-Aza-CdR, providing a mechanistic explanation for the importance of combinatorial therapy in eliciting maximal de-repression of the cancer epigenome.

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