Horticultural Sciences Department, Plant Molecular and Cellular Biology Program, University of Florida, Gainesville, Florida 32611.
Plant Physiol. 2013 Nov;163(3):1293-305. doi: 10.1104/pp.113.220988. Epub 2013 Sep 16.
The transition between seed and seedling phases of development is coordinated by an interaction between the closely related ABSCISIC ACID-INSENSITIVE3 (ABI3), FUSCA3 (FUS3), and LEAFY COTYLEDON2 (LEC2; AFL) and VIVIPAROUS1/ABI3-LIKE (VAL) clades of the B3 transcription factor family that respectively activate and repress the seed maturation program. In the val1 val2 double mutant, derepression of the LEC1, LEC1-LIKE (L1L), and AFL (LAFL) network is associated with misexpression of embryonic characteristics resulting in arrested seedling development. We show that while the frequency of the embryonic fate in val1 val2 seedlings depends on the developmental timing of seed rescue, VAL proteins repress LAFL genes during germination, but not during seed development. Quantitative analysis of LAFL mutants that suppress the val1 val2 seedling phenotype revealed distinct roles of LAFL genes in promoting activation of the LAFL network. LEC2 and FUS3 are both essential for coordinate activation of the network, whereas effects of LEC1, L1L, and ABI3 are additive. Suppression of the val1 val2 seedling phenotype by the B3 domain-deficient abi3-12 mutation indicates that ABI3 activation of the LAFL network requires the B3 DNA-binding domain. In the VAL-deficient background, coordinate regulation of the LAFL network is observed over a wide range of genetic and developmental conditions. Our findings highlight distinct functional roles and interactions of LAFL network genes that are uncovered in the absence of VAL repressors.
发育过程中种子到幼苗阶段的转变是由密切相关的脱落酸不敏感 3（ABI3）、FUSCA3（FUS3）和 LEAFY COTYLEDON2（LEC2；AFL）与 VIVIPAROUS1/ABI3-LIKE（VAL）B3 转录因子家族的分支之间的相互作用来协调的，该家族分别激活和抑制种子成熟程序。在 val1 val2 双突变体中，LEC1、LEC1-LIKE（L1L）和 AFL（LAFL）网络的去抑制与胚胎特征的异常表达有关，导致幼苗发育停滞。我们表明，虽然 val1 val2 幼苗中胚胎命运的频率取决于种子挽救的发育时间，但 VAL 蛋白在萌发过程中抑制 LAFL 基因，但不在种子发育过程中抑制。对抑制 val1 val2 幼苗表型的 LAFL 突变体的定量分析揭示了 LAFL 基因在促进 LAFL 网络激活中的不同作用。LEC2 和 FUS3 对于网络的协调激活都是必需的，而 LEC1、L1L 和 ABI3 的作用是累加的。abi3-12 突变体缺失 B3 结构域抑制 val1 val2 幼苗表型表明，ABI3 对 LAFL 网络的激活需要 B3 DNA 结合结构域。在 VAL 缺陷背景下，在广泛的遗传和发育条件下观察到 LAFL 网络的协调调控。我们的研究结果突出了在没有 VAL 抑制剂的情况下，LAFL 网络基因的不同功能作用和相互作用。
