PIN-FORMED1 and PINOID regulate boundary formation and cotyledon development in Arabidopsis embryogenesis
PIN-FORMED1 and PINOID regulate boundary formation and cotyledon development in Arabidopsis embryogenesis
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DOI：
10.1242/dev.01388
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发表时间：
2004-10-01
期刊：
影响因子：
4.6
通讯作者：
Aida, M
中科院分区：
文献类型：
--
作者：
Furutani, M;Vernoux, T;Aida, M
在双子叶植物中，在胚的顶端区域的两侧对称位置形成两个子叶。介导生长素依赖性器官形成的PIN-FORMED 1（PIN 1）和PINE 1（PID）基因的单突变适度破坏子叶的对称模式。我们报告说，pin 1 pid双突变体显示出一个惊人的表型，完全缺乏子叶和双边对称。在双突变体胚中，杯形子叶1（CUC 1）、CUC 2和无茎芽（STM）的表达结构域（其功能通常需要抑制子叶边界处的生长）扩展到外周并与子叶特异性标记丝状花重叠。消除CUC 1，CUC 2或STM活性导致恢复子叶生长的双突变体，这表明这些边界基因的负调控PIN 1和PID是足够的原基生长。我们还表明PID mRNA主要定位于子叶原基的边界，并且PID mRNA的早期表达依赖于PIN。我们的研究结果证明了PIN和PID在建立双侧对称性以及促进子叶生长中的冗余作用，后者涉及到边界特异性下游效应子CUC 1，CUC 2和STM基因的负调控。
In dicotyledonous plants, two cotyledons are formed at bilaterally symmetric positions in the apical region of the embryo. Single mutations in the PIN-FORMED1 (PIN1) and PINOID (PID) genes, which mediate auxin-dependent organ formation, moderately disrupt the symmetric patterning of cotyledons. We report that the pin1 pid double mutant displays a striking phenotype that completely lacks cotyledons and bilateral symmetry. In the double mutant embryo, the expression domains of CUP-SHAPED COTYLEDON1 (CUC1), CUC2 and SHOOT MERISTEMLESS (STM), the functions of which are normally required to repress growth at cotyledon boundaries, expand to the periphery and overlap with a cotyledon-specific marker, FILAMENTOUS FLOWER. Elimination of CUC1, CUC2 or STM activity leads to recovery of cotyledon growth in the double mutant, suggesting that the negative regulation of these boundary genes by PIN1 and PID is sufficient for primordium growth. We also show that PID mRNA is localized mainly to the boundaries of cotyledon primordia and early expression of PID mRNA is dependent on PIN]. Our results demonstrate the redundant roles of PIN] and PID in the establishment of bilateral symmetry, as well as in the promotion of cotyledon outgrowth, the latter of which involves the negative regulation of CUC1, CUC2 and STM genes, which are boundary-specific downstream effectors.