背景回顾：In monocarpic plants, all reproductive meristem activity arrests and flower production ceases after the production of a certain number of fruits. This proliferative arrest (PA) is an evolutionary adaptation that ensures nutrient availability for seed production. Moreover, PA is a process of agronomic interest because it affects the duration of the flowering period and therefore fruit production. 

提出问题：While our knowledge of the inputs and genetic factors controlling the initiation of the flowering period is extensive, little is known about the regulatory pathways and cellular events that participate in the end of flowering and trigger PA.

主要研究：Here, we characterize with high spatiotemporal resolution the cellular and molecular changes related to cell proliferation and meristem activity in the shoot apical meristem throughout the flowering period and PA. 

结果1-CK抑制PA：Our results suggest that cytokinin (CK) signaling repression precedes PA and that this hormone is sufficient to prevent and revert the process. 

结果2-CK下游WUS：We have also observed that repression of known CK downstream factors, such as type B cyclins and WUSCHEL (WUS), correlates with PA. These molecular changes are accompanied by changes in cell size and number likely caused by the cessation of cell division and WUS activity during PA. 

结果3-FUL抑制CK，促进PA：Parallel assays in fruitfull (ful) mutants, which do not undergo PA, have revealed that FUL may promote PA via repression of these CK-dependent pathways. 

结果4-Two phases：Moreover, our data allow to define two phases, based on the relative contribution of FUL, that lead to PA: an early reduction ofCK-related events and a late blocking of these events.

 摘 要 

在单次结实的植物中，在产生一定数量的果实后，所有生殖分生组织活性和开花都会停止。这种增殖停滞（proliferative arrest）是一种演化适应性性状，能够保证种子发育和成熟所需的充分养分。此外，增殖停滞也是比较重要的农艺性状，因为其影响了开花的持续时间和果实的产量。尽管，目前我们对于控制开花时间起始的遗传因素已经研究得比较深入了，但是对于参与开花终止和诱导增殖停滞的调控通路和细胞事件还所知甚少。本文中，作者鉴定了开花过程和增值停滞阶段茎尖分生组织中，与细胞增殖和分生组织活性相关的高时空分辨率细胞和分子改变。作者的研究结果显示，细胞分裂素CK信号转导的抑制要先于增殖停滞，并且CK便足以阻止或逆转增殖停滞这一过程。作者还发现type B细胞周期蛋白和WUS等CK已知的下游因子的抑制与增殖停滞相关。这些分子改变总伴随着细胞大小和数量的改变，很有可能是增殖停滞过程中细胞分裂和WUS活性停止所导致的。ful突变体并不存在增殖停滞这一过程，在该突变体中的平行试验显示，FUL可能通过对CK依赖型通路的抑制来促进增殖停滞。此外，本文的数据基于FUL对增殖停滞的相对贡献，定义了两个阶段：早期CK相关的事件减少和晚期这些事件的阻断。

 通讯作者 

** Cristina Ferrándiz **