The FUS3 transcription factor functions through the epidermal regulator TTG1 during embryogenesis in Arabidopsis

被引:84
作者
Tsuchiya, Y
Nambara, E
Naito, S
McCourt, P
机构
[1] Univ Toronto, Dept Bot, Toronto, ON, Canada
[2] Hokkaido Univ, Grad Sch Agr, Div Appl Biosci, Sapporo, Hokkaido 0608589, Japan
[3] RIKEN, Plant Sci Ctr, Lab Reprod Growth Regulat, Wako, Saitama 3510198, Japan
关键词
plant development; late embryogenesis; leafy cotyledons;
D O I
10.1046/j.1365-313X.2003.01939.x
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
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.
引用
收藏
页码:73 / 81
页数:9
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