Cellular redox, epigenetics and diseases.

Since the Central dogma of Molecular Biology was proposed about 40 years ago; our understanding of the intricacies of gene regulation has undergone tectonic shifts almost every decade. It is now widely accepted that the complexity of an organism is not directed by the sheer number of genes it carries but how they are decoded by a myriad of regulatory modules. Over the years, it has emerged that the organizations chromatins and its remodeling; splicing and polyadenylation of pre-mRNAs, stability and localization of mRNAs and modulation of their expression by non-coding and miRNAs play pivotal roles in metazoan gene expression. Nevertheless, in spite of tremendous progress in our understanding of all these mechanisms of gene regulation, the way these events are coordinated leading towards a highly defined proteome of a given cell type remains enigmatic. In that context, the structures of many metazoan genes cannot fully explain their pattern of expression in different tissues, especially during embryonic development and progression of various diseases. Further, numerous studies done during the past quarter of a century suggested that the heritable states of transcriptional activation or repression of a gene can be influenced by the covalent modifications of constituent bases and associated histones; its chromosomal context and long-range interactions between various chromosomal elements (Holliday 1987; Turner 1998; Lyon 1993). However, molecular dissection of these phenomena is largely unknown and is an exciting topic of research under the sub-discipline epigenetics (Gasser et al. 1998).