Arabidopsis nucleoporin CPR5 controls trichome cell death through the core cell cycle regulator CKI
Arabidopsis nucleoporin CPR5 controls trichome cell death through the core cell cycle regulator CKI
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拟南芥核孔蛋白CPR5通过核心细胞周期调节因子CKI控制毛状体细胞死亡
DOI：
10.1111/plb.13068
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发表时间：
2019
期刊：
影响因子：
3.9
通讯作者：
Shui Wang
中科院分区：
文献类型：
--
作者：
Shun Peng;Keke Sun;Yuan Guo;Yunhan Liu;Shui Wang
拟南芥表皮毛是由多轮胞内循环形成的多倍性表皮细胞。胞苷酸依赖激酶抑制剂（CKI）家族蛋白是促进内循环的核心细胞周期调节剂。PR基因的组成型表达5（CPR 5）是植物特异性的核孔蛋白。已经发现，拟南芥CKI中的两种，SIAMESE（SIM）和SIAMESE-RELATED 1（SMR 1），在CPR 5的下游起作用以激活植物效应子触发的细胞死亡。sim smr 1双突变体形成多细胞和簇状毛状体，而cpr 5突变体产生死的和无分支的毛状体。本研究探讨了CPR 5-CKI信号通路在毛状体细胞周期转换中的作用。为了研究植物毛状体细胞周期转换如何调节的潜在机制，进行了台盼蓝染色、流式细胞术、扫描电子显微镜（SEM）和核DNA测量。天然启动子驱动的CKI和GUS融合报告基因表明SIM和SMR 1蛋白都优先在毛状体中表达。cpr 5诱导的死的和无分支的毛状体被SIM SMR 1双突变体完全抑制，表明SIM和SMR 1在毛状体发育中CPR 5的下游起作用。流式细胞仪分析显示，与2C（C是单倍体核中的DNA含量）细胞数量相比，cpr 5突变体中4C细胞的数量显着增加，而多倍细胞（8 C和16 C）的数量显着减少。cpr 5突变体中升高的4C/2C比率与前内循环调节剂SIM和SMR 1的去阻遏一致。多倍性细胞（8 C和16 C）可以选择性地靶向细胞死亡，这因此归因于cpr 5突变体中的无分支毛状体。细胞核DNA含量分析表明，cpr 5 sim突变体的毛状体细胞核DNA含量显著高于sim突变体，表明CPR 5是毛状体细胞核内循环的负调控因子。本研究揭示了CPR 5-CKI信号通路控制着植物毛状体细胞周期的转换，过量的内循环是植物毛状体细胞死亡所必需的。
Arabidopsis trichome is a polyploidy epidermal cell resulting from multiple rounds of the endocycles. The CYCLIN-DEPENDENT KINASE INHIBITOR (CKI) family proteins are core cell cycle regulators which promote endocycle. CONSTITUTIVE EXPRESSION OF PR GENES 5 (CPR5) is a plant-specific nucleoporin. It has been found that two of Arabidopsis CKIs, SIAMESE (SIM) and SIAMESE-RELATED 1 (SMR1), function downstream of CPR5 to activate plant effector-triggered cell death. The sim smr1 double mutants form multicellular and clustered trichomes, while the cpr5 mutants produce dead and branchless trichomes. This study explored roles of the CPR5-CKI signaling pathway in trichome cell cycle transition..To examine the underlying mechanism of how cell cycle transition is regulated in plant trichome, Trypan Blue staining, flow cytometry, scanning electron microscopy (SEM) and nuclear DNA measurement were conducted..The native promoter-driven CKI and GUS fusion reporter showed that both SIM and SMR1 proteins were preferentially expressed in trichome. The cpr5-induced dead and branchless trichomes were fully suppressed by the sim smr1 double mutant, suggesting that SIM and SMR1 function downstream of CPR5 in trichome development. Flow cytometry analysis showed that as compared to the number of 2C (C is the DNA content in a haploid nucleus) cells, the number of 4C cells significantly increased, whereas that of polyploidy cells (8C and 16C) dramatically decreased in the cpr5 mutant. The elevated 4C/2C ratio in cpr5 mutant is consistent with derepression of pro-endocycle regulators SIM and SMR1. The polyploidy cells (8C and 16C) may be selectively targeted to cell death which is therefore attributed to the branchless trichomes in cpr5 mutant. Nuclear DNA content analysis demonstrated that the nuclear DNA content of trichome in cpr5 sim mutant was significantly higher than that in sim mutant, indicating that CPR5 is a negative endocycle regulator in trichome. .This study reveals that the CPR5-CKI signaling pathway controls trichome cell cycle transition and excessive endocycle is required for cell death in plant trichome.