Role of vacuolar-type proton pump in compensated cell enlargement

生物学中一个长期存在的问题是器官大小是如何预先确定的。补偿是一个关键的，但尚未解决的现象，从而细胞数量减少低于一定的阈值触发增强有丝分裂后细胞的叶原基的扩张。从而为研究叶片大小控制提供了一个典型案例。在表现出补偿作用的拟南芥突变体中，我在这里集中研究了液泡型H^+-焦磷酸酶（H^+-PPase）缺陷的fugu 5突变体。我清楚地证明了PPi在胞质溶胶中的高积累介导了Fugu 5中的细胞再生妥协，提供了PPi水解是Fugu 5在体内的主要作用的证据。此外，我进行了一个大规模的筛选fugu 5突变体的增强子，抑制子和抑制子，并确定了三个突变株，影响细胞扩增fugu 5以不同的方式。最后，我发现V-ATP酶与在fugu 2 -1和KRP 2 o/e中观察到的过度细胞增大有关。

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.