Department of Biological Sciences, Indian Institute of Science Education and Research (IISER), Bhopal, 462066, India.
Institute of Biology/Applied Genetics, Dahlem Centre of Plant Sciences (DCPS), Freie Univeristät Berlin, Albrecht-Thaer-Weg 6, Berlin, D-14195, Germany.
Plant J. 2020 Jul;103(2):481-496. doi: 10.1111/tpj.14844. Epub 2020 Jun 17.
Under acute stress conditions, precocious seedling development may result in the premature death of young seedlings, before they switch to autotrophic growth. The phytohormone abscisic acid (ABA) inhibits seed germination and post-germination seedling establishment under unfavorable conditions. Various environmental signals interact with the ABA pathway to optimize these early developmental events under stress. Here, we show that light availability critically influences ABA sensitivity during early seedling development. In dark conditions, the ABA-mediated inhibition of post-germination seedling establishment is strongly enhanced. COP1, a central regulator of seedling development in the dark, is necessary for this enhanced post-germination ABA sensitivity in darkness. Despite their slower germination, cop1 seedlings establish faster than wild type in the presence of ABA in both light and dark. PHY and CRY photoreceptors that inhibit COP1 activity in light modulate ABA-mediated inhibition of seedling establishment in light. Genetically, COP1 acts downstream to ABI5, a key transcriptional regulator of ABA signaling, and does not influence the transcriptional and protein levels of ABI5 during the early post-germination stages. COP1 promotes post-germination growth arrest independent of the antagonistic interaction between ABA and cytokinin signaling pathways. COP1 facilitates the binding of ABI5 on its target promoters and the ABA-mediated upregulation of these target genes is reduced in cop1-4. Together, our results suggest that COP1 positively regulates ABA signaling to inhibit post-germination seedling establishment under stress.
在急性胁迫条件下，早熟的幼苗发育可能导致幼苗在向自养生长转变之前过早死亡。植物激素脱落酸（ABA）抑制不利条件下种子的萌发和萌发后幼苗的建立。各种环境信号与 ABA 途径相互作用，以优化胁迫下这些早期发育事件。在这里，我们表明光照可用性在早期幼苗发育过程中对 ABA 敏感性具有重要影响。在黑暗条件下，ABA 对萌发后幼苗建立的抑制作用大大增强。COP1 是黑暗中幼苗发育的中央调节剂，是这种增强的黑暗中萌发后 ABA 敏感性所必需的。尽管 cop1 幼苗的萌发速度较慢，但在光照和黑暗中，cop1 幼苗在 ABA 存在下的建立速度比野生型快。PHY 和 CRY 光受体在光照下抑制 COP1 活性，调节光照下 ABA 对幼苗建立的抑制作用。从遗传上讲，COP1 作用于 ABI5 下游，ABI5 是 ABA 信号转导的关键转录调节剂，在萌发后的早期阶段，COP1 不会影响 ABI5 的转录和蛋白水平。COP1 促进萌发后生长停滞，不依赖于 ABA 和细胞分裂素信号通路的拮抗相互作用。COP1 促进 ABI5 与其靶启动子的结合，COP1-4 中 ABA 介导的这些靶基因的上调减少。总之，我们的研究结果表明，COP1 正向调控 ABA 信号，以抑制胁迫下萌发后幼苗的建立。
