首页 | 本学科首页   官方微博 | 高级检索  
     


Class III compensation,represented by KRP2 overexpression,depends on V-ATPase activity in proliferative cells
Authors:Ali Ferjani  Kazuki Ishikawa  Mariko Asaoka  Masanori Ishida  Gorou Horiguchi  Masayoshi Maeshima  Hirokazu Tsukaya
Affiliation:1.Department of Biology; Tokyo Gakugei University; Koganei-shi, Japan;2.Laboratory of Cell Dynamics; Graduate School of Bioagricultural Sciences; Nagoya University; Nagoya, Japan;3.Department of Life Science; College of Science; Rikkyo University; Nishi-Ikebukuro, Japan;4.Research Center for Life Science; College of Science; Rikkyo University; Nishi-Ikebukuro, Japan;5.Department of Biological Sciences; Graduate School of Science; University of Tokyo; Bunkyo-ku, Japan
Abstract:Compensation refers to an increase in cell size when the cell number is significantly decreased due to the mutation or gain of function of a gene that negatively affects the cell cycle. Given the importance of coordinated growth during organogenesis in both animal and plant systems, compensation is important to understand the mechanism of size regulation. In leaves, cell division precedes cell differentiation (which involves cell expansion); therefore, a decrease in cell number triggers enhanced cell expansion (compensated cell expansion; hereafter, CCE). Functional analyses of genes for which a loss or gain of function triggers compensation have increased our understanding of the molecular mechanisms underlying the decrease in cell number. Nevertheless, the mechanisms that induce enhanced cell expansion (the link between cell cycling and expansion), as well as the cellular machinery mediating CCE, have not been characterized. We recently characterized an important pathway involved in cell enlargement in KRP2-overexpressing plants. Here, we discuss the potential role of plant KRPs in triggering enlargement in cells with meristematic features.
Keywords:Arabidopsis   leaf development   cell size   organ-size regulation   compensation   KRP2   V-ATPase   det3-1
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号