背景回顾：Fruit malformation is a major constrain in fruit production world-wide resulting in substantial economic losses. The farmers for decades noticed that the chilling temperature prior to the blooming often caused malformed fruits.  

提出问题：However, the molecular mechanism underlying this phenomenon is unclear. 

结果1-低温诱导胼胝质积累：Here we examined the fruit development in response to cold stress in tomato, and demonstrated that short-term cold stress increased the callose accumulation in both shoot apical and floral meristems, resulting in the symplastic isolation and altered intercellular movement of WUS. 

结果2-WUS胞间移动被阻断：In contrast to the rapidly restored SlWUS transcription during the recovery from cold stress, the callose removal was delayed due to obstructed plasmodesmata. 

结果3-WUS反馈回路阻断：The delayed reinstatement of cell-to-cell transport of SlWUSprevented the activation of SlCLV3 and TAG1, causing the interrupted feedback-inhibition of SlWUS expression, leading to the expanded stem cell population and malformed fruits. 

结果4-胼胝质动态调控机制：We further showed that the callose dynamics in response to short-term cold stress presumably exploits the mechanism of bud dormancy during the seasonal growth, involving two antagonistic hormones ABA and GA. 

结论：Our results provide a novel insight into the cold stress regulated malformation of fruit.

果实畸形是全球范围内水果生产的主要制约因素，造成了巨大的经济损失。农民们在几十年的种植过程中已经注意到，开花前经历低温往往会导致果实畸形。但是，该现象潜在的分子机制并不清晰。本文中，作者研究了番茄果实响应于低温胁迫的发育，发现短期低温胁迫增加了茎尖和花分生组织中的胼胝质积累，导致了共质体隔离，改变了WUS的胞间迁移。与低温恢复期间SlWUS转录的快速恢复相反，由于胞间连丝受阻，胼胝质的去除延迟发生。SlWUS蛋白胞间转运的延迟恢复阻碍了SlCLV3和TAG1的激活，导致了SlWUS表达反馈抑制的扰乱，最终导致干细胞群的扩张以及果实畸形。作者进一步发现，在生长季响应于短期低温胁迫的胼胝质动态可能利用了芽休眠的机制，涉及到ABA和GA两种植物激素之间的拮抗。本文的研究结果为低温导致的果实畸形提供了新的视野。

** 吴 双 **