期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2021
卷号：118
期号：33
DOI：10.1073/pnas.2107558118
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Significance
Low phosphate (Pi) availability is a major constraint for plant productivity in both natural and agricultural environments. Over the course of evolution, plants acquired a complex cascade of transcriptional responses that enhance their capacity to survive and reproduce in phosphate-poor soils. However, it is unclear to what extent chromatin architecture is modified to activate or repress gene expression in response to Pi starvation. Here, we report the effects of Pi starvation on chromatin accessibility and its association with gene expression. We determined that major remodeling in chromatin accessibility takes place in response to Pi starvation and that this response is activated by the PHR1 family of transcription factors.
As phosphorus is one of the most limiting nutrients in many natural and agricultural ecosystems, plants have evolved strategies that cope with its scarcity. Genetic approaches have facilitated the identification of several molecular elements that regulate the phosphate (Pi) starvation response (PSR) of plants, including the master regulator of the transcriptional response to phosphate starvation PHOSPHATE STARVATION RESPONSE1 (PHR1). However, the chromatin modifications underlying the plant transcriptional response to phosphate scarcity remain largely unknown. Here, we present a detailed analysis of changes in chromatin accessibility during phosphate starvation in
Arabidopsis thaliana root cells. Root cells undergo a genome-wide remodeling of chromatin accessibility in response to Pi starvation that is often associated with changes in the transcription of neighboring genes. Analysis of chromatin accessibility in the
phr1 phl2 double mutant revealed that the transcription factors PHR1 and PHL2 play a key role in remodeling chromatin accessibility in response to Pi limitation. We also discovered that PHR1 and PHL2 play an important role in determining chromatin accessibility and the associated transcription of many genes under optimal Pi conditions, including genes involved in the PSR. We propose that a set of transcription factors directly activated by PHR1 in Pi-starved root cells trigger a second wave of epigenetic changes required for the transcriptional activation of the complete set of low-Pi–responsive genes.
