Fujikura Ushio, Horiguchi Gorou, Ponce María Rosa, Micol José Luis, Tsukaya Hirokazu
Graduate School of Science, Faculty of Science, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Plant J. 2009 Aug;59(3):499-508. doi: 10.1111/j.1365-313X.2009.03886.x. Epub 2009 Apr 6.
Co-ordination of cell proliferation and cell expansion is a key regulatory process in leaf-size determination, but its molecular details are unknown. In Arabidopsis thaliana, mutations in a positive regulator of cell proliferation often trigger excessive cell enlargement post-mitotically in leaves. This phenomenon, called compensation syndrome, is seen in the mutant angustifolia3 (an3), which is defective in a transcription co-activator. Such compensation, however, does not occur in response to a decrease in cell number in oligocellula (oli). oli2, oli5 and oli7 did not exhibit compensation and the reduction in cell number in these mutants was moderate. However, when an oli mutation was combined with a different oli mutation to create a double mutant, cell number was further reduced and compensation was induced. Similarly, weak suppression of AN3 expression reduced cell number moderately but did not induce compensation compared with an an3 null mutant. Furthermore, double mutants of either oli2, oli5 or oli7 and an3 showed markedly enhanced compensation. These results suggest that compensation is triggered when cell proliferation regulated by OLI2/OLI5/OLI7 and AN3 is compromised in a threshold-dependent manner. OLI2 encodes a Nop2 homolog in Saccharomyces cerevisiae that is involved in ribosome biogenesis, whereas OLI5 and OLI7 encode ribosome proteins RPL5A and RPL5B, respectively. This suggests that a factor involved in the induction of compensation may be under the dual control of AN3 and a ribosome-related process.
细胞增殖与细胞扩张的协调是叶片大小决定中的一个关键调控过程,但其分子细节尚不清楚。在拟南芥中,细胞增殖正调控因子的突变常常在叶片有丝分裂后触发细胞过度增大。这种现象被称为补偿综合征,在转录共激活因子有缺陷的突变体狭叶3(an3)中可见。然而,在少细胞(oli)突变体中,细胞数量减少时并不会发生这种补偿。oli2、oli5和oli7没有表现出补偿现象,这些突变体中的细胞数量减少幅度适中。然而,当一个oli突变与另一个不同的oli突变结合产生双突变体时,细胞数量进一步减少并诱导出补偿现象。同样,与an3无效突变体相比,AN3表达的弱抑制适度减少了细胞数量,但没有诱导出补偿现象。此外,oli2、oli5或oli7与an3的双突变体表现出明显增强的补偿现象。这些结果表明,当由OLI2/OLI5/OLI7和AN3调控的细胞增殖以阈值依赖的方式受到损害时,补偿现象就会被触发。OLI2编码酿酒酵母中一种参与核糖体生物合成的Nop2同源物,而OLI5和OLI7分别编码核糖体蛋白RPL5A和RPL5B。这表明参与诱导补偿的一个因子可能受到AN3和核糖体相关过程的双重控制。