Cells of a multicellular organism are genetically identical but differ in structure and function. This heterogeneity is created by several epigenetic mechanisms during the development of the organism. The epigenetic changes- including DNA methylation, histone post-translational modifications, chromatin remodeling and RNA interference have all been shown to control chromatin structure and regulate a plethora of cellular and organismal processes. There is a strong evidence that epigenetics play a crucial role in the development of diseases such as cancer, schizophrenia or metabolic disorders. The epigenetic regulation underlie memory formation or adaptation to external stimuli. The extent to which environmental effects can provoke epigenetic responses represents an exciting area of future research. Here we review the current knowledge about the epigenetic mechanisms and their relation to the human health and disease.
In flowering plants, seeds are produced both sexually (double fertilization is required) and asexually via apomixis (meiotic reduction and egg fertilization are omitted). An apomictic-like pattern of endosperm development in planta is followed by fis mutants of sexual Arabidopsis thaliana. In our experiments in planta, autonomous endosperm (AE) developed in met1 mutants. Furthermore we obtained autonomous endosperm formation in vitro not only in unfertilized ovules of fie mutants but also in wild genotypes (Col-0, MET1/MET1, FIE/FIE) and met1 mutants. AE induction and development occurred in all genotypes on the each of the media used and in every trial. The frequency of AE was relatively high (51.2% ovaries) and genotype-dependent. AE induced in vitro represents a more advanced stage of development than AE induced in fie mutants in planta. This was manifested by a high number of nuclei surrounded by cytoplasm and organized in nuclear cytoplasmic domains (NCDs), nodule formation, division into characteristic regions, and cellularization. The high frequency of AE observed in homozygous met1 (met1/met1) mutants probably is due to accumulation of hypomethylation as an effect of the met1 mutation and the in vitro conditions. AE development was most advanced in FIE/fie mutants. We suggest that changes in the methylation of one or several genes in the DNA of Arabidopsis genotypes caused by in vitro conditions resulted in AE induction and/or further AE development.