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：2016
卷号：113
期号：51
页码：E8335-E8343
DOI：10.1073/pnas.1610670114
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：SignificanceLight, a prevailing environmental factor, plays important roles in various processes during plant development and stress response. Whether light could also regulate stress-induced transcriptional memory, however, is not clear. Herein we reported that light signal is positively involved in salt-induced transcriptional memory of {Delta}1-pyrroline-5-carboxylate synthetase 1 (P5CS1) and subsequent proline accumulation. Furthermore, HY5-dependent light signaling is required for the maintenance of salt-induced H3K4me3 in P5CS1 during the recovery stage. This mechanism is likely operating during other stress as well, and could shed light on future research into the concerted effects of different environmental factors on plant response to stresses. To cope with environmental stresses, plants often adopt a memory response upon primary stress exposure to facilitate a quicker and stronger reaction to recurring stresses. However, it remains unknown whether light is involved in the manifestation of stress memory. Proline accumulation is a striking metabolic adaptation of higher plants during various environmental stresses. Here we show that salinity-induced proline accumulation is memorable and HY5-dependent light signaling is required for such a memory response. Primary salt stress induced the expression of {Delta}1-pyrroline-5-carboxylate synthetase 1 (P5CS1), encoding a proline biosynthetic enzyme and proline accumulation, which were reduced to basal level during the recovery stage. Reoccurring salt stress-induced stronger P5CS1 expression and proline accumulation were dependent upon light exposure during the recovery stage. Further studies demonstrated that salt-induced transcriptional memory of P5CS1 is associated with the retention of increased H3K4me3 level at P5CS1 during the recovery stage. HY5 binds directly to light-responsive element, C/A-box, in the P5CS1 promoter. Deletion of the C/A-box or hy5 hyh mutations caused rapid reduction of H3K4me3 level at P5CS1 during the recovery stage, resulting in impairment of the stress memory response. These results unveil a previously unrecognized mechanism whereby light regulates salt-induced transcriptional memory via the function of HY5 in maintaining H3K4me3 level at the memory gene.
