关键词: FLOWERING LOCUS T THYLAKOID FORMATION 1 chloroplast flowering temperature

来  源:   DOI:10.1111/tpj.16970

Abstract:
The intracellular localization of the florigen FLOWERING LOCUS T (FT) is important for its long-distance transport toward the shoot apical meristem. However, the mechanisms regulating the FT localization remain poorly understood. Here, we discovered that in Arabidopsis thaliana, the chloroplast-localized protein THYLAKOID FORMATION 1 (THF1) physically interacts with FT, sequestering FT in the outer chloroplast envelope. Loss of THF1 function led to temperature-insensitive flowering, resulting in early flowering, especially under low ambient temperatures. THF1 mainly acts in the leaf vasculature and shoot apex to prevent flowering. Mutation of CONSTANS or FT completely suppressed the early flowering of thf1-1 mutants. FT and THF1 interact via their anion binding pocket and coiled-coil domain (CCD), respectively. Deletion of the CCD in THF1 by gene editing caused temperature-insensitive early flowering similar to that observed in the thf1-1 mutant. FT levels in the outer chloroplast envelope decreased in the thf1-1 mutant, suggesting that THF1 is important for sequestering FT. Furthermore, THF1 protein levels decreased in seedlings grown at high ambient temperature, suggesting an explanation for its role in plant responses to ambient temperature. A thf1-1 phosphatidylglycerolphosphate synthase 1 (pgp1) double mutant exhibited additive acceleration of flowering at 23 and 16°C, compared to the single mutants, indicating that THF1 and phosphatidylglycerol (PG) act as independent but synergistic regulators of temperature-responsive flowering. Collectively, our results provide an understanding of the genetic pathway involving THF1 and its role in temperature-responsive flowering and reveal a previously unappreciated additive interplay between THF1 and PG in temperature-responsive flowering.
摘要:
FflorigenFLOWERINGLOCUST(FT)的细胞内定位对于其向茎尖分生组织的长距离运输很重要。然而,调节FT本地化的机制仍然知之甚少。这里,我们发现在拟南芥中,叶绿体定位的蛋白质THYLAKOID形成1(THF1)与FT物理相互作用,在叶绿体外膜中螯合FT。THF1功能的丧失导致温度不敏感的开花,导致早期开花,特别是在低环境温度下。THF1主要作用于叶片脉管系统和茎尖以防止开花。CONSTANS或FT的突变完全抑制了thf1-1突变体的早期开花。FT和THF1通过其阴离子结合袋和卷曲螺旋结构域(CCD)相互作用,分别。通过基因编辑删除THF1中的CCD会导致对温度不敏感的早期开花,与thf1-1突变体中观察到的相似。在thf1-1突变体中,外叶绿体包膜中的FT水平降低,这表明THF1对隔离FT很重要。此外,在高环境温度下生长的幼苗中THF1蛋白水平降低,为其在植物对环境温度的反应中的作用提供了解释。thf1-1磷脂酰甘油磷酸合酶1(pgp1)双突变体在23和16°C时表现出开花的累加加速,与单一突变体相比,表明THF1和磷脂酰甘油(PG)是温度响应性开花的独立但协同的调节剂。总的来说,我们的结果提供了涉及THF1的遗传途径及其在温度响应性开花中的作用的理解,并揭示了温度响应性开花中THF1和PG之间先前未被理解的加性相互作用。
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