Arabidopsis LEAFY COTYLEDON1 Mediates Postembryonic Development via Interacting with PHYTOCHROME-INTERACTING FACTOR4
Arabidopsis LEAFY COTYLEDON1 Mediates Postembryonic Development via Interacting with PHYTOCHROME-INTERACTING FACTOR4
复制标题
拟南芥 LEAFY COTYLEDON1 通过与 PHYTOCHROME-INTERACTING FACTOR4 相互作用介导胚胎后发育
DOI：
10.1105/tpc.15.00750
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发表时间：
2015-11-01
期刊：
影响因子：
11.6
通讯作者：
Hou, Xingliang
中科院分区：
文献类型：
--
作者：
Huang, Mingkun;Hu, Yilong;Hou, Xingliang
植物在从萌发种子到幼苗的发育过程中经历胚后生长。最近的研究表明，LEAFY COTYLEDON1(LEC1)最初被认为是拟南芥胚胎发生和种子成熟的中央调节因子，在胚胎后发育中发挥着独特的作用。然而，LEC1调控非胚胎发育的机制仍然不清楚。在这项研究中，我们观察了LEC1突变体和可诱导的LEC1过表达转基因系的早期幼苗的黄化相关表型。与此一致的是，LEC1以一种黑暗依赖的方式促进下胚轴伸长相关基因的表达，尽管在光照和黑暗生长的幼苗中LEC1的转录水平相似。此外，我们还发现LEC1与萌发后发育中的主要转录调节因子光敏色素相互作用因子4(PIF4)相互作用，通过在黑暗中直接与G-box元件结合来相互调控下胚轴伸长相关基因。此外，LEC1功能的丧失抑制了PIF过度积累植物的伸长下胚轴表型；相反，LEC1的诱导过表达并不能挽救PIF4突变体中的短下胚轴。我们的发现表明，LEC1在胚胎后生长过程中作为PIFs的辅助激活因子，为植物在从胚胎期到幼苗建立的转变过程中微调形态发育提供了一种可能的机制。
Plants undergo postembryonic growth during the developmental transition from germinating seeds to seedlings. Recent studies suggest LEAFY COTYLEDON1 (LEC1), initially identified as a central regulator in embryogenesis and seed maturation in Arabidopsis thaliana, plays a distinct role in postembryonic development. However, the mechanism by which LEC1 regulates nonembryonic development still remains elusive. In this study, we observed etiolation-related phenotypes in early seedlings of lec1 mutants and inducible LEC1 overexpression transgenic lines. Consistent with this, LEC1 promotes the expression of hypocotyl elongation-related genes in a darkness-dependent manner in spite of the comparable LEC1 transcript levels in the light- and dark-grown seedlings. Furthermore, we show that LEC1 interacts with PHYTOCHROME-INTERACTING FACTOR4 (PIF4), a major transcription modulator in postgermination development, to interdependently regulate hypocotyl elongation-related genes via direct binding to G-box element in the dark. Moreover, loss of LEC1 function suppresses the elongated hypocotyl phenotype of PIF-overaccumulating plants; conversely, inducible overexpression of LEC1 does not rescue the short hypocotyl in pif4 mutants. Our findings reveal that LEC1 acts as a coactivator of PIFs in transcriptional regulation during postembryonic growth, providing a possible mechanism by which plants fine-tune morphological development for their survival during the transition from the embryonic phase to seedling establishment.