Department of Ornamental Horticulture, China Agricultural University, Beijing, 100193, China.
Plant J. 2014 Sep;79(6):941-50. doi: 10.1111/tpj.12594. Epub 2014 Jul 28.
Drought is a major abiotic stress that affects the development and growth of most plants, and limits crop yield worldwide. Although the response of plants to drought has been well documented, much less is known about how plants respond to the water recovery process, namely rehydration. Here, we describe the spatio-temporal response of plant reproductive organs to rehydration using rose flowers as an experimental system. We found that rehydration triggered rapid and transient ethylene production in the gynoecia. This ethylene burst serves as a signal to ensure water recovery in flowers, and promotes flower opening by influencing the expression of a set of rehydration-responsive genes. An in-gel kinase assay suggested that the rehydration-induced ethylene burst resulted from transient accumulation of RhACS1/2 proteins in gynoecia. Meanwhile, RhMPK6, a rose homolog of Arabidopsis thaliana MPK6, is rapidly activated by rehydration within 0.5 h. Furthermore, RhMPK6 was able to phosphorylate RhACS1 but not RhACS2 in vitro. Application of the kinase inhibitor K252a suppressed RhACS1 accumulation and rehydration-induced ethylene production in gynoecia, and the protein phosphatase inhibitor okadaic acid had the opposite effect, confirming that accumulation of RhACS1 was phosphorylation-dependent. Finally, silencing of RhMPK6 significantly reduced ethylene production in gynoecia when flowers were subjected to rehydration. Taken together, our results suggest that temporal- and spatial-specific activation of an RhMPK6-RhACS1 cascade is responsible for rehydration-induced ethylene production in gynoecia, and that the resulting ethylene-mediated signaling pathway is a key factor in flower rehydration.
干旱是一种主要的非生物胁迫,影响大多数植物的发育和生长,并限制了全球作物的产量。尽管植物对干旱的反应已有详细的记录,但对于植物如何响应水恢复过程,即再水合,了解甚少。在这里,我们使用玫瑰花作为实验系统描述了植物生殖器官对再水合的时空响应。我们发现,再水合在雌蕊中迅速引发短暂的乙烯产生。这种乙烯爆发作为一种信号,以确保花朵中的水分恢复,并通过影响一组再水合反应基因的表达来促进花朵开放。凝胶激酶测定表明,再水合诱导的乙烯爆发是由于 RhACS1/2 蛋白在雌蕊中的瞬时积累。同时,RhMPK6,拟南芥 MPK6 的玫瑰同源物,在 0.5 小时内被再水合迅速激活。此外,RhMPK6 在体外能够磷酸化 RhACS1 但不能磷酸化 RhACS2。激酶抑制剂 K252a 的应用抑制了 RhACS1 在雌蕊中的积累和再水合诱导的乙烯产生,而蛋白磷酸酶抑制剂 okadaic acid 则产生相反的效果,证实了 RhACS1 的积累是依赖于磷酸化的。最后,当花朵再水合时,沉默 RhMPK6 显著降低了雌蕊中的乙烯产生。总之,我们的结果表明,RhMPK6-RhACS1 级联的时空特异性激活负责雌蕊中再水合诱导的乙烯产生,而由此产生的乙烯介导的信号通路是花朵再水合的关键因素。