Key Laboratory of Plant Molecular Physiology, CAS Center for Excellence in Molecular Plant Sciences, Institute of Botany, Chinese Academy of Sciences, Beijing 100093, China.
Key Laboratory of Plant Molecular Physiology, CAS Center for Excellence in Molecular Plant Sciences, Institute of Botany, Chinese Academy of Sciences, Beijing 100093, China; University of Chinese Academy of Sciences, Beijing 100049, China.
Cell Rep. 2021 May 11;35(6):109095. doi: 10.1016/j.celrep.2021.109095.
Dicotyledonous plants form an apical hook to protect the fragile apical meristem during upward protrusion from the soil. Etiolated pifq (pif1 pif3 pif4 pif5) seedlings display constitutive apical hook opening. Here, we show that PIF proteins control apical hook opening by regulating the expression of Budding Uninhibited by Benzimidazole 3.1 (BUB3.1) and affecting cytokinesis. Consistent with the major function of BUB3.1 in the organization of phragmoplasts during cytokinesis, the phragmoplasts are well formed in dark-grown pifq but not in wild type. DNA staining and flow cytometry analysis further demonstrate that cellular endoreduplication levels are dramatically reduced in pifq. Chemical treatment with caffeine, an inhibitor of phragmoplast-based cytokinesis, shows that cytokinesis is involved in the apical hook opening. Genetically, BUB3.1 is epistatic to PIFq in the regulation of cytokinesis. Our findings reveal an organ-specific role of PIF proteins in regulating cytokinesis by BUB3.1 during apical hook development.
双子叶植物在向上突出土壤的过程中形成一个顶端钩，以保护脆弱的顶端分生组织。黄化的 pifq（pif1 pif3 pif4 pif5）幼苗表现出组成型顶端钩张开。在这里，我们表明 PIF 蛋白通过调节增殖细胞核抗原 3.1（BUB3.1）的表达和影响细胞分裂来控制顶端钩的张开。与 BUB3.1 在细胞分裂过程中组织胞质分裂板的主要功能一致，暗培养的 pifq 中胞质分裂板形成良好，而在野生型中则不然。DNA 染色和流式细胞术分析进一步表明，pifq 中的细胞内内复制水平显著降低。用咖啡因（一种基于胞质分裂板的细胞分裂抑制剂）进行化学处理表明，细胞分裂参与了顶端钩的张开。遗传上，BUB3.1 在调控细胞分裂方面对 PIFq 具有上位性。我们的发现揭示了 PIF 蛋白在顶端钩发育过程中通过 BUB3.1 调节细胞分裂的器官特异性作用。
