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Abstract：
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.
摘要：
双子叶植物在从土壤向上突出期间形成顶端钩以保护脆弱的顶端分生组织。黄体化的pifq（pif1pif3pif4pif5）幼苗显示出组成型根尖钩开口。这里,我们表明，PIF蛋白通过调节苯并咪唑3.1（BUB3.1）未抑制的芽的表达和影响胞质分裂来控制顶端钩的开放。与BUB3.1在胞质分裂过程中的原生质体组织中的主要功能一致，原生质体在深色生长的pifq中形成良好，但在野生型中却没有。DNA染色和流式细胞术分析进一步证明细胞内复制水平在pifq中显著降低。用咖啡因化学处理，一种基于原生质体的胞质分裂的抑制剂，显示胞质分裂参与顶端钩开口。基因上,BUB3.1在胞质分裂的调节中对PIFq具有上位性。我们的发现揭示了PIF蛋白在根尖钩发育过程中通过BUB3.1调节胞质分裂中的器官特异性作用。
