The regulation of leaf size has been studied for decades. Enhancement of post-mitotic cell expansion triggered by impaired cell proliferation in Arabidopsis is an important process for leaf size regulation, and is known as compensation. This suggests a key interaction between cell proliferation and cell expansion during leaf development. Several studies have highlighted the impact of this integration mechanism on leaf size determination; however, the molecular basis of compensation remains largely unknown. Previously, we identified extra-small sisters (xs) mutants which can suppress compensated cell enlargement (CCE) via a specific defect in cell expansion within the compensation-exhibiting mutant, angustifolia3 (an3). Here we revealed that one of the xs mutants, namely xs2, can suppress CCE not only in an3 but also in other compensation-exhibiting mutants erecta (er) and fugu2. Molecular cloning of XS2 identified a deleterious mutation in CATION CALCIUM EXCHANGER 4 (CCX4). Phytohormone measurement and expression analysis revealed that xs2 shows hyper activation of the salicylic acid (SA) response pathway, where activation of SA response can suppress CCE in compensation mutants. All together, these results highlight the regulatory connection which coordinates compensation and SA response.

几十年来，人们一直在研究叶片大小的调节。拟南芥细胞增殖受损引发的有丝分裂后细胞扩张增强是调节叶片大小的重要过程，被称为补偿。这表明在叶发育过程中细胞增殖和细胞扩张之间存在关键的相互作用。几项研究强调了这种整合机制对叶片大小确定的影响；然而，补偿的分子基础在很大程度上仍然未知。以前，我们发现了超小姐妹( xs ) 突变体，这些突变体可以通过补偿性突变体angustifolia3 ( an3 ) 中细胞扩增的特定缺陷来抑制补偿性细胞增大 (CCE)). 在这里，我们揭示了xs突变体之一，即xs2，不仅可以抑制an3中的 CCE ，还可以抑制其他补偿性突变体erecta ( er ) 和fugu2中的 CCE 。XS2的分子克隆鉴定出CATION CALCIUM EXCHANGER 4 ( CCX4 )中的有害突变。植物激素测量和表达分析显示xs2显示水杨酸 (SA) 反应通路的过度激活，其中 SA 反应的激活可以抑制补偿突变体中的 CCE。总之，这些结果突出了协调补偿和 SA 响应的监管联系。