Plants, unlike animals, can’t move, and have to respond to various environmental signals (such as seasonal changes) which often cause various modifications to plant genomes, including DNA methylation and histone modifications. Some of these marks can be transmitted through cell divisions to regulate gene expression and thus plant growth and development. To ensure the proper development of offspring, these marks must be erased in gametes or early embryos.
The seasonal cue winter cold (or prolonged exposure to cold temperatures) through a process termed as vernalization enables some plants to flower in next spring when temperature rises. In previous study of the model plant Arabidopsis thaliana, winter cold triggers histone modifications at FLOWERING LOCUS C (FLC, a potent floral repressor) to shut down its expression, which renders plants competent to flower in the coming spring.
This silenced FLC chromatin state is maintained in spring, but is reset in offspring so that next generation needs to be vernalized again. The mechanism 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 group led by Prof. HE Yuehui at Shanghai Institute of Plant Physiology and Ecology, CAS Center for Excellence in Molecular Plant Sciences of Chinese Academy of Sciences (CAS), uncovered an embryonic epigenetic reprogramming mechanism by a pioneer transcription factor. The study was published in Nature.
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, they 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.
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).
52 Sanlihe Rd., Beijing,