Journal of Genetics and DNA Research

Understudying epigenetics underlying mechanisms is essential. Studies have indicated functional roles of epigenetic events, including DNA methylation and histone modifications, in human disease, stem cell growth and development, aging, response to environmental stresses, and species evolution. High-throughput sequencing techniques alongside routine experimental approaches have rapidly produced a bulk of data that the major part of them remained unprocessed. To analyze, interpret, and process of these data, availability of efficient computational methods is critical. Epigenetic data analysis is complex and difficult because these data contain multi-layer set of information. The methods implemented to this purpose must be able to handle massive data of experimental works and process the epigenetic layers. Furthermore, the methods must be capable of integrating multiple modifications and their combination effects on chromatin conformational structure and consequently the expression network of genes. In this study, we briefly reviewed challenges in the way of the computational epigenetics, the latest reported methods, and significant biological results derived from Appling computational-based methods on epigenetic data.

Non-syndromic orofacial malformations do not manifest any symptoms. Various signaling pathways are important in lip and palate development, but the specific genes in these pathways that play a role in causing oral clefts in humans remain unknown. Orofacial clefts are related to 14q chromosome with its associated candidate genes like ISGF3G at 14q11.2, JAG2 at 14q32, PAX9 at 14q13.3, TGFB3 at 14q24.3 and BMP4 at 14q22. Previous studies excluded the pathways linked to candidate genes and their role in formation of orofacial clefts. Linkage pathways of specific genes involved in formation of orofacial malformations are not well established in humans due to different varieties of approach. More studies need to be established in understanding the pathways linked to candidate genes involved in orofacial malformations.

This angstroms to ecosystems model of ecological adaptation links nutrient energy-dependent epigenetic effects on base pairs and amino acid substitutions to pheromone-controlled changes in the microRNA/messenger RNA balance and chromosomal rearrangements via the physiology of reproduction in species from microbes to humans. The nutrient-dependent pheromone-controlled changes are required for the thermodynamic regulation of intracellular signaling, which enables biophysically constrained nutrient-dependent protein folding; experiencedependent receptor-mediated behaviors, and organism-level thermoregulation in ever-changing ecological niches and social niches. Nutrient-dependent ecological, social, neurogenic and socio-cognitive niche construction are manifested in increasing organismal complexity. Species-specific pheromones link quorum-sensing in microbes from chemical ecology to the physiology of reproduction. The reciprocal relationships of species-typical nutrientdependent morphological and behavioral diversity are enabled by pheromone-controlled reproduction. Ecological variations and biophysically constrained natural selection for codon optimality links nutritional epigenetics to the behaviors that enable ecological adaptations. All biodiversity is an ecologically validated proof-of-concept. Ideas from population genetics, which exclude ecological factors, are integrated with an experimental evidence-based approach that establishes what is currently known. Simply put, olfactory/pheromonal input links food odors and social odors from the epigenetic landscape to the physical landscape of supercoiled DNA in the organized genomes of species from microbes to man during their development.