CUC1 gene activates the expression of SAM-related genes to induce adventitious shoot formation
CUC1 gene activates the expression of SAM-related genes to induce adventitious shoot formation
复制标题
DOI：
10.1046/j.1365-313x.2003.01911.x
复制
发表时间：
2003-12-01
期刊：
影响因子：
7.2
通讯作者：
Tasaka, M
中科院分区：
文献类型：
--
作者：
Hibara, K;Takada, S;Tasaka, M
杯形子叶（CUC）1编码NAC家族的成员。这些基因在拟南芥胚胎发生过程中参与茎尖分生组织（SAM）的形成和子叶的分离。我们分析了过表达CUC 1（35 S：：CUC 1）的转基因植物。这些转基因幼苗的子叶有规律地具有两个基部裂片，窦之间的小而圆的表皮细胞，以及在该区域的近轴面上的不定SAM。这表明CUC 1通过维持表皮细胞处于未分化状态来促进外源SAM形成。在35 S：：CUC 1子叶中，与SAM形成和/或维持有关的类结样同源盒基因（KNOX），包括SHOOT MERISTEMLESS（STM）和BREVIPEDICELLUS（BP），在不定SAM形成前异位表达。在stm突变体中，CUC 1的异位表达不能诱导外源SAM，而它们继续在bp突变体中观察到。这些结果表明，STM，而不是BP，是必要的35 S：：CUC 1子叶中的不定SAM的形成。此外，我们研究了CUC 1和不对称叶（AS）1和AS 2之间的关系。as 1和as 2突变基因增强35 S：：CUC 1表型，即使在STM功能的情况下。有趣的是，as 1突变可以部分挽救cuc 1 cuc 2双突变体中的突变体营养发育表型。我们的研究结果表明，CUC 1正调控SAM的形成不仅通过STM，但也通过STM-独立的途径，是负调控的AS 1和AS 2。
CUP-SHAPED COTYLEDON (CUC)1 encodes members of the NAC family. These are functionally redundant genes that are involved in shoot apical meristem (SAM) formation and cotyledon separation during embryogenesis in Arabidopsis. We analyzed transgenic plants overexpressing CUC1 (35S::CUC1). The cotyledons of these transgenic seedlings regularly had two basal lobes, small and round epidermal cells between the sinuses, and adventitious SAMs on the adaxial surface of this region. This suggests that CUC1 promotes adventitious SAM formation by maintaining epidermal cells in an undifferentiated state. In 35S::CUC1 cotyledons, the class I knotted-like homeobox (KNOX) genes, including SHOOT MERISTEMLESS (STM) and BREVIPEDICELLUS (BP), which are involved in SAM formation and/or maintenance, were ectopically expressed before adventitious SAM formation. In stm mutants, ectopic expression of CUC1 could not induce adventitious SAMs, whereas they continued to be observed in bp mutants. These results suggest that STM, but not BP, is necessary for the formation of adventitious SAMs in 35S::CUC1 cotyledons. Furthermore, we examined the relationship between CUC1 and ASYMMETRIC LEAVES (AS)1 and AS2. The as1 and as2 mutations genetically enhance 35S::CUC1 phenotypes even in the absence of STM function. Interestingly, the as1 mutation can partially rescue the mutant vegetative development phenotypes in the cuc1 cuc2 double mutant. Our results suggest that CUC1 positively regulates SAM formation not only through STM but also through an STM-independent pathway that is negatively regulated by AS1 and AS2.