Tsuchiya Yuichiro, Nambara Eiji, Naito Satoshi, McCourt Peter
Department of Botany, University of Toronto, 25 Willcocks Street, Toronto, Ontario, Canada.
Plant J. 2004 Jan;37(1):73-81. doi: 10.1046/j.1365-313x.2003.01939.x.
Loss-of-function mutations in the FUSCA3 (FUS3) gene of Arabidopsis result in alterations in cotyledon identity, inability to complete late seed maturation processes, and the premature activation of apical and root embryonic meristems, which indicates that this transcription factor is an essential regulator of embryogenesis. Although FUS3 shows a complex pattern of expression in the embryo, this gene is only required in the protoderm to carry out its functions. Moreover, the epidermal morphogenesis regulator TRANSPARENT TESTA GLABRA1 (TTG1) is negatively regulated by FUS3 in the embryo. When a loss-of-function ttg1 mutation is introduced into a fus3 mutant, a number of fus3-related phenotypes are rescued, indicating a functional TTG1 gene is required to manifest the fus3 mutant phenotype. It therefore appears that one of the functions of FUS3 is to restrict the domain of expression of TTG1 during embryogenesis. The FUS3-TTG1 interaction is both maternal and zygotic, suggesting a complex relationship is required between these gene products to allow correct seed development.
拟南芥中FUSCA3（FUS3）基因的功能丧失突变会导致子叶特征改变、无法完成种子后期成熟过程以及顶端和根胚胎分生组织的过早激活，这表明该转录因子是胚胎发育的重要调节因子。尽管FUS3在胚胎中表现出复杂的表达模式，但该基因仅在原表皮中发挥功能时才是必需的。此外，表皮形态发生调节因子透明种皮光滑1（TTG1）在胚胎中受到FUS3的负调控。当将功能丧失的ttg1突变引入fus3突变体时，许多与fus3相关的表型得以挽救，这表明功能性TTG1基因是表现fus3突变体表型所必需的。因此，FUS3的功能之一似乎是在胚胎发育过程中限制TTG1的表达域。FUS3与TTG1的相互作用既有母本效应又有合子效应，这表明这些基因产物之间需要一种复杂的关系来确保种子的正常发育。
