Chrysanthemum is a typical short day (SD) flowering plant that requires a longer night period than a critical minimum duration to successfully flower. We identified FLOWERING LOCUS T-LIKE 3 (FTL3) and ANTI-FLORIGENIC FT/TFL1 FAMILY PROTEIN (AFT) as a florigen and antiflorigen, respectively, in a wild diploid chrysanthemum (Chrysanthemum seticuspe). Expression of the genes that produce these proteins, CsFTL3 and CsAFT, is induced in the leaves under SD or a noninductive photoperiod, respectively, and the balance between them determines the progression of floral transition and anthesis. However, how CsFTL3 and CsAFT are regulated to define the critical night length for flowering in chrysanthemum is unclear. In this study, we focused on the circadian clock-related gene GIGANTEA (GI) of C. seticuspe (CsGI) and generated transgenic C. seticuspe plants overexpressing CsGI (CsGI-OX). Under a strongly inductive SD (8 L/16D) photoperiod, floral transition occurred at almost the same time in both wild-type and CsGI-OX plants. However, under a moderately inductive (12 L/12D) photoperiod, the floral transition in CsGI-OX plants was strongly suppressed, suggesting that the critical night length for flowering was lengthened for CsGI-OX plants. Under the 12 L/12D photoperiod, CsAFT was upregulated in CsGI-OX plants. Giving a night break (NB) 10 h after dusk was the most effective time to inhibit flowering in wild-type plants, while the most effective time for NB was extended to dawn (12 and 14 h after dusk) in CsGI-OX plants. In wild-type plants, a red-light pulse delivered 8 or 10 h after dusk induced maximal CsAFT expression, but the length of the time period over which CsAFT could be induced by red light was extended until subjective dawn in CsGI-OX plants. Therefore, CsGI-OX plants required a longer dark period to maintain lower levels of CsAFT, and their critical night length for flowering was thus lengthened. These results suggested that CsGI has an important role in the control of photoperiodic flowering through shaping the gate for CsAFT induction by light in chrysanthemum.

中文翻译：

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CsGI的组成型表达通过改变菊花抗成花素诱导的光敏期来改变开花的临界夜长

菊花是典型的短日照 (SD) 开花植物，需要比临界最短持续时间更长的夜间才能成功开花。我们在野生二倍体菊花 (Chrysanthemum seticuspe) 中分别将 FLOWERING LOCUS T-LIKE 3 (FTL3) 和 ANTI-FLORIGENIC FT/TFL1 家族蛋白 (AFT) 鉴定为成花剂和抗成花剂。产生这些蛋白质的基因 CsFTL3 和 CsAFT 的表达分别在 SD 或非诱导光周期下的叶子中被诱导，它们之间的平衡决定了花的过渡和开花的进程。然而，如何调节 CsFTL3 和 CsAFT 以定义菊花开花的关键夜间长度尚不清楚。在这项研究中，我们专注于 C. seticuspe (CsGI) 的生物钟相关基因 GIGANTEA (GI) 并生成了转基因 C. 过表达 CsGI (CsGI-OX) 的 seticuspe 植物。在强诱导 SD (8 L/16D) 光周期下，野生型和 CsGI-OX 植物几乎同时发生花期转变。然而，在适度诱导 (12 L/12D) 光周期下，CsGI-OX 植物的花期转变受到强烈抑制，表明 CsGI-OX 植物开花的临界夜间长度延长。在 12 L/12D 光周期下，CsGI-OX 植物中的 CsAFT 上调。在黄昏后 10 小时休息 (NB) 是抑制野生型植物开花的最有效时间，而在 CsGI-OX 植物中，NB 的最有效时间延长至黎明（黄昏后 12 小时和 14 小时）。在野生型植物中，黄昏后 8 或 10 小时发出红光脉冲，诱导最大的 CsAFT 表达，但红光诱导 CsAFT 的时间段延长到 CsGI-OX 植物主观黎明。因此，CsGI-OX 植物需要更长的黑暗期来维持较低的 CsAFT 水平，从而延长了它们开花的临界夜间长度。这些结果表明，CsGI 通过塑造菊花光诱导 CsAFT 的门，在控制光周期开花中具有重要作用。