Research Reveals Embryonic Resetting of Parental Epigenetic Marks in Plants
Plants, unlike animals, can’t move, and have to respond to various environmental signals (such as seasonal changes) and biotic and abiotic stresses. These environmental inputs will often cause various modifications to plant genomes (made of DNA and histone proteins), including DNA methylation and histone modifications. Some of these marks can be transmitted through cell divisions, and these epigenetic marks play a central role in regulation of gene expression and thus growth and development in plants. To ensure the proper development of offspring, these marks must be erased in gametes or early embryos.
In many plant species, when to flower is controlled by environmental cues. At high latitudes, winter cold or prolonged exposure to cold temperatures, through a process termed as vernalization, enables plants to flower in next spring when temperature rises and days become longer. Previous study of model flowering plant Arabidopsis thaliana demonstrated that winter cold ‘shuts down’ the expression of a potent floral repressor FLOWERING LOCUS C (FLC), and renders plants competent to flower in the coming spring. Winter cold triggers repressive histone modifications on FLC chromatin leading to FLC silencing. This silencing state is maintained after the plants return to warm (spring), but is reset in offspring so that next generation needs winter-cold exposure again in order to flower in spring. However, the mechanisms of how parental histone marks are erased in plants offspring and how the silenced FLC is reset in next generation remain unclear.
Recently, a research team led by Prof. HE Yuehui at the Shanghai Center for Plant Stress Biology (PSC), Shanghai Institute of Plant Physiology and Ecology (SIPPE), CAS Center for Excellence in Molecular Plant Sciences, Chinese Academy of Sciences (CAS), has uncovered an embryonic epigenetic reprogramming mechanism by a pioneer transcription factor.
In this study, the researchers discovered that shortly after fertilization a seed-specific pioneer transcription factor known as LEC1 can promote the initial establishment of an active chromatin state at FLC and function to de novo activate FLC expression. LEC1 engages embryonic chromatin modifiers to establish the active state, resulting in the reversing of the silenced chromatin state inherited from gametes. Furthermore, the researchers found that the active chromatin state at the FLC locus is passed on from the pro-embryo to post-embryonic stages where new organs such as leaves are continuously formed. This enables an embryonic or seed-specific factor acting to ‘control’ post-embryonic development processes, for instance, when a plant to flower in adult stage.
The results revealed a novel mechanism for how environment-induced epigenetic marks on parental genomes are reset in offspring and delineate an epigenetic mechanism for a seed-specific factor to exert control on post-seed life.
The work, entitled “Embryonic epigenetic reprogramming by a pioneer transcription factor in plants”, was published in Nature on October 26, 2017.
This study was supported in part by the National Key Research and Development Program of China, the Chinese Academy of Sciences and the Temasek Life Sciences Laboratory (Singapore).
HE Yuehui, Principal Investigator
Shanghai Center for Plant Stress Biology (PSC)
Shanghai Institute of Plant Physiology and Ecology (SIPPE)
CAS Center for Excellence in Molecular Plant Sciences
Chinese Academy of Sciences (CAS)
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