Although cytokinins (CKs) regulate fruit development, no direct genetic evidence supports the role of endogenous CKs in pericarp growth or development or fruit size. Here, we report that the reduction in endogenous active CKs level via overexpression of a CKs-inactivating enzyme gene AtCKX2 specifically in fruit tissues resulted in reduced pericarp thickness and smaller fruit size, compared to wild-type control fruits. The pericarp thickness and single fruit weight in transgenic plants were significantly reduced. Analysis of paraffin sections showed that the reduced pericarp thickness was due largely to a decreased number of cells, and thus decreased cell division. Transcriptome profiling showed that the expression of cell division- and expansion-related genes was reduced in AtCKX2-overexpressing fruits. In addition, the expression of auxin-signaling and gibberellin-biosynthetic genes was repressed, whereas that of gibberellin-inactivating genes was enhanced, in AtCKX2-overexpressing fruits. These results demonstrate that endogenous CKs regulate pericarp cell division and, subsequently, fruit size. They also suggest that CKs interact with auxin and gibberellins in regulating tomato pericarp thickness and fruit size.

中文翻译：

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细胞分裂素参与调节番茄果皮厚度和果实大小。


尽管细胞分裂素 (CK) 调节果实发育，但没有直接的遗传证据支持内源 CK 在果皮生长或发育或果实大小中的作用。在这里，我们报告说，与野生型对照水果相比，通过特异地在水果组织中过表达 CKs 失活酶基因 AtCKX2 来降低内源活性 CKs 水平，导致果皮厚度减少和水果尺寸变小。转基因植株果皮厚度和单果重显着降低。石蜡切片分析表明，果皮厚度减少主要是由于细胞数量减少，从而减少了细胞分裂。转录组分析表明，AtCKX2 过表达的果实中细胞分裂和扩增相关基因的表达降低。此外，在AtCKX2过表达的果实中，生长素信号传导基因和赤霉素生物合成基因的表达受到抑制，而赤霉素失活基因的表达则增强。这些结果表明，内源 CK 调节果皮细胞分裂，进而调节果实大小。他们还表明，CK 与生长素和赤霉素相互作用，调节番茄果皮厚度和果实大小。