One of the most critical epigenetic signatures present in the genome of higher eukaryotes is the methylation of DNA at the C-5 position of the cytosine ring. Based on the sites of DNA methylation in a locus, it can serve as a repressive or activation mark for gene expression. In a crosstalk with histone modifiers, DNA methylation can consequently either inhibit binding of the transcription machinery or generate a landscape conducive for transcription. During developmental phases, the DNA methylation pattern in the genome undergoes alterations as a result of regulated balance between de novo DNA methylation and demethylation. Resultantly, differentiated cells inherit a unique DNA methylation pattern that fine tunes tissue-specific gene expression. Although apparently a stable epigenetic mark, DNA methylation is actually labile and is a complex reflection of interaction between epigenome, genome and environmental factors prior to birth and during progression of life. Recent findings indicate that levels of DNA methylation in an individual is a dynamic outcome, strongly influenced by the dietary environment during germ cell formation, embryogenesis and post birth exposures. Loss of balances in DNA methylation during developmental stages may result in imprinting disorders, while at any later stage may lead to increased predisposition to various diseases and abnormalities. This review aims to provide an outline of how our epigenome is uniquely guided by our lifetime of experiences beginning in the womb and how understanding it better holds future possibilities of improvised clinical applications.
The transcription factor abscisic acid insensitive 3 (ABI3) has recently been shown to mediate the dehydration stress response in nonseed and seed plants by regulation of several downstream genes. Here, we show how ABI3 autoregulates its transcription in response to dehydration stress signalling. Autoactivation is primarily through the Sph/RY element CATGCA present at the promoter region of ABI3. Along with other known cis-elements found at the ABI3 promoter, CATGCA remains occluded by nucleosomes during transcription repression. The nucleosomes tend to reposit during active transcription and are associated with several histone modifications, such as H3K9 and K27 acetylations and H3K4 trimethylation. This work thus, reveals the genetic and epigenetic essentials required for expression of the ABI3 gene, a crucial factor regulating dehydration stress signalling in Arabidopsis thaliana.
Developmental plasticity and the ability to regenerate organs during the life cycle are a signature feature of plant system. De novo organogenesis is a common mode of plant regeneration and may occur directly from the explant or indirectly via callus formation. It is now evident that callus formation occurs through the root development pathway. In fact, callus cells behave like a group of root primordium cells that are under the control of exogenous auxin. Presence or absence of auxin decides the subsequent fate of these cells. While in presence of external supplementation of auxin they are maintained as root primordia cells, absence of exogenous auxin induces the callus cells into patterning, differentiation and finally root emergence. Here we show that in absence of functional ABI3, a prominent member of the B3 superfamily of transcription factors, root regeneration is compromised in Arabidopsis callus cells. In culture medium free of any exogenous hormone supplementation, while adventitious root emergence and growth was prominently observed in wild type cells, no such features were observed in abi3-6 cells. Expression of auxin-responsive AUX1 and GH3 genes was significantly reduced in abi3-6 cells, indicating that auxin levels or distribution may be altered in absence of ABI3.
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