Szymkowiak Eugene J, Irish Erin E
Department of Biological Sciences, The University of Iowa, Iowa City, 52246, USA.
Planta. 2006 Mar;223(4):646-58. doi: 10.1007/s00425-005-0115-x. Epub 2005 Oct 1.
Unlike monopodial plants, in which flowering terminates growth of a shoot, plants exhibiting sympodial shoot architecture maintain the potential for indeterminate growth even after converting to floral development. This vegetative indeterminacy is conferred by a special type of axillary meristem, the sympodial meristem, which exhibits precocious but determinate growth. The reiterative formation of sympodial meristems as the plant grows results in a shoot composed of a series of modules, each consisting of a limited number of vegetative nodes and terminated by a flower or inflorescence. To determine how sympodial meristems differ from other shoot meristems, we examined interactions between mutations that affect various shoot meristem types in tomato (Lycopersicon esculentum Mill.). Analysis of double mutant combinations of jointless, lateral suppressor, self-pruning, blind, and anantha showed that sympodial meristems share regulatory features with inflorescence meristems. Genetic studies on the jointless mutation implicated this gene in suppressing sympodial meristem fate in the inflorescence. As this mutation has a second phenotype, the elimination of the pedicel abscission zone, we examined the expression pattern of JOINTLESS to test whether pedicel development is involved in directing shoot architecture. We found that this MADS box gene is expressed in a variety of shoot meristems, including inflorescence, floral, sympodial, and axillary meristems, as well as in early staged floral organs, in sporogenous tissues of anthers, and in ovules. Lack of expression in developing pedicels indicates abscission zone development does not rely on JOINTLESS transcription in the differentiating cells. We conclude that the primary role of JOINTLESS is to suppress sympodial meristem identity in inflorescence meristems.
与单轴植物不同，在单轴植物中开花会终止茎的生长，而具有合轴茎结构的植物即使在转变为花发育后仍保持无限生长的潜力。这种营养生长的不确定性是由一种特殊类型的腋生分生组织——合轴分生组织赋予的，它表现出早熟但有限的生长。随着植物生长，合轴分生组织的反复形成导致茎由一系列模块组成，每个模块由有限数量的营养节组成，并以一朵花或一个花序结束。为了确定合轴分生组织与其他茎分生组织有何不同，我们研究了影响番茄（Lycopersicon esculentum Mill.）各种茎分生组织类型的突变之间的相互作用。对无节、侧芽抑制、自剪、盲芽和无花的双突变组合的分析表明，合轴分生组织与花序分生组织具有共同的调控特征。对无节突变的遗传研究表明，该基因参与抑制花序中的合轴分生组织命运。由于这个突变有第二个表型，即花梗离层区的消失，我们研究了无节基因的表达模式，以测试花梗发育是否参与指导茎的结构。我们发现这个MADS盒基因在多种茎分生组织中表达，包括花序、花、合轴和腋生分生组织，以及早期的花器官、花药的孢子发生组织和胚珠。在发育中的花梗中缺乏表达表明离层区的发育不依赖于分化细胞中的无节基因转录。我们得出结论，无节基因的主要作用是抑制花序分生组织中的合轴分生组织特性。
