Arabidopsis LEAFY COTYLEDON1 controls cell fate determination during post-embryonic development
Arabidopsis LEAFY COTYLEDON1 controls cell fate determination during post-embryonic development
复制标题
拟南芥LEAFY COTYLEDON1控制胚胎后发育过程中的细胞命运决定
DOI：
10.3389/fpls.2015.00955
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发表时间：
2015-11-03
影响因子：
5.6
通讯作者：
Hou, Xingliang
中科院分区：
文献类型：
--
作者：
Huang, Mingkun;Hu, Yilong;Hou, Xingliang
拟南芥LEAFY COTYLEDON1(LEC1)转录因子是植物胚胎发育和胚后幼苗建立的主要调控因子。LEC1功能的丧失改变了子叶的特性，导致异位毛状体的形成，这在野生型幼苗中不存在，这意味着LEC1可能调控胚胎细胞在胚胎后发育过程中的命运决定。为了验证这一假设，我们比较了野生型和lec1突变体之间毛状体发育相关基因的表达。我们观察到，编码毛状体发育正调控基因GLABROUS1(GL1)、GL2和GL3的转录显著上调，而编码毛状体发育负调控基因的TRICHOMELESS1(TCL2)、TRY和CPC1增强子(ETC1)和ETC2基因在lec1突变体中表达下调。此外，LEC1的过表达激活了TCL2、CAPPICE(CPC)和ETC1的表达，导致营养发育过程中子叶无毛或少毛。此外，我们还证明了LEC1与TCL2在酵母和体外都有相互作用。一项遗传实验表明，GL2功能的丧失挽救了lec1突变体中异位毛状体的形成。这些发现有力地支持了LEC1对毛状体发育的调控，为LEC1在胚胎后发育过程中决定细胞命运提供了直接证据。
Arabidopsis LEAFY COTYLEDON1 (LEC1) transcription factor is a master regulator that shapes plant embryo development and post-embryonic seedling establishment. Loss-of-function of LEC1 alters the cotyledon identity, causing the formation of ectopic trichomes, which does not occur in wild-type seedlings, implying that LEC1 might regulate embryonic cell fate determination during post-embryonic development. To test this hypothesis, we compared the expression of trichome development-related genes between the wild-type and the lec1 mutant. We observed that transcripts of GLABROUS1 (GL1), GL2, and GL3, genes encoding the positive regulators in trichome development, were significantly upregulated, while the TRICHOMELESS1 (TCL2), ENHANCER OF TRY AND CPC1 (ETC1), and ETC2 genes, encoding the negative regulators in trichome development, were downregulated in the lec1 mutant. Furthermore, overexpression of LEC1 activated the expressions of TCL2, CAPPICE (CPC), and ETC1, resulting in production of cotyledonary leaves with no or fewer trichomes during vegetative development. In addition, we demonstrated that LEC1 interacts with TCL2 in yeast and in vitro. A genetic experiment showed that loss-of-function of GL2 rescued the ectopic trichome formation in the lec1 mutant. These findings strongly support that LEC1 regulates trichome development, providing direct evidence for the role of LEC1 in cell fate determination during post-embryonic development.