Role of vacuolar-type proton pump in compensated cell enlargement

生物学中一个由来已久的问题是器官大小是如何预先确定的。补偿是一个关键但尚未解决的现象，即细胞数量低于某个阈值时，会触发叶原基中有丝分裂后细胞扩张的增强。从而为研究烟叶大小控制提供了一个模式案例。在拟南芥中表现出补偿的突变体中，我重点介绍了液泡型H^+-焦磷酸酶(H^+-PPase)缺陷突变体Fugu5。我清楚地证明了胞浆中PPI的高度积累介导了FUGU5的糖异生妥协，提供了PPI水解是FUGU5在体内的主要作用的证据。此外，我还对fugu5突变体的增强子、抑制子和抑制子进行了大规模的筛选，并鉴定了三个以不同方式影响fugu5细胞扩张的突变株。最后，我发现V-ATPase与Fugu2-1和KRP2 o/e中观察到的细胞过度增大有关。

A longstanding question in biology is how organ size is predetermined. Compensation is a key, yet unsolved phenomenon, whereby decreased cell number below some threshold triggers enhanced post-mitotic cell expansion in leaf primordia. Thus providing a model case to investigate leaf-size control. Among the Arabidopsis mutants that exhibit compensation, here I focused on fugu5 mutant that is defective in vacuolar-type H^+-pyrophosphatase (H^+-PPase). I clearly demonstrated that high accumulation of PPi in the cytosol mediates gluconeogenesis compromise in fugu5, providing evidence that PPi hydrolysis is the major role of FUGU5 in vivo. Also, I conducted a large-scale screening of enhancers, repressors and suppressors of fugu5 mutant and identified three mutant lines that affect cell expansion in fugu5 in different manners. Finally, I found that V-ATPase is implicated in excessive cell enlargement observed in fugu2-1 and KRP2 o/e.