GIGAS CELL1, a Novel Negative Regulator of the Anaphase-Promoting Complex/Cyclosome, Is Required for Proper Mitotic Progression and Cell Fate Determination in Arabidopsis
GIGAS CELL1, a Novel Negative Regulator of the Anaphase-Promoting Complex/Cyclosome, Is Required for Proper Mitotic Progression and Cell Fate Determination in Arabidopsis
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DOI：
10.1105/tpc.111.092049
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发表时间：
2011-12-01
期刊：
影响因子：
11.6
通讯作者：
Ito, Masaki
中科院分区：
文献类型：
--
作者：
Iwata, Eriko;Ikeda, Saki;Ito, Masaki
细胞倍性的增加在多细胞生物的发育过程中是普遍存在的，特别是在植物中。倍性水平的升高通常是通过内复制或内质分裂来实现的，这通常被认为是完全或部分缺乏M期的修饰细胞周期。我们鉴定了GIGAS CELL1 (GIG1)/遗漏的第二分裂1 (OSD1)，并确定该基因突变引发异位子宫内膜增多症。另一方面，据报道，GIG1/OSD1的类似物UV-INSENSITIVE4 （UVI4）负调控拟南芥内复制的发生。研究人员发现，GIG1/OSD1和UVI4编码新的植物后期促进复合物/环体（APC/C）泛素连接酶特异性抑制剂。在酵母双杂交实验中，这些蛋白与APC/C激活因子CDC20/FZY和CDH1/FZR发生物理相互作用。CDC20.1和CCS52B/FZR3的过表达差异促进了gig1/osd1的异位内膜增生和uvi4的早期内复制。我们的数据表明，GIG1/OSD1和UVI4可能分别通过优先抑制APC/C-CDC20和APC/C-FZR来阻止细胞倍性的非计划性增加。在gig1/osd1中产生混合身份的细胞进一步表明，APC/C除了在有丝分裂过程中发挥作用外，还可能在细胞命运决定中发挥意想不到的作用。
Increased cellular ploidy is widespread during developmental processes of multicellular organisms, especially in plants. Elevated ploidy levels are typically achieved either by endoreplication or endomitosis, which are often regarded as modified cell cycles that lack an M phase either entirely or partially. We identified GIGAS CELL1 (GIG1)/OMISSION OF SECOND DIVISION1 (OSD1) and established that mutation of this gene triggered ectopic endomitosis. On the other hand, it has been reported that a paralog of GIG1/OSD1, UV-INSENSITIVE4 (UVI4), negatively regulates endoreplication onset in Arabidopsis thaliana. We showed that GIG1/OSD1 and UVI4 encode novel plant-specific inhibitors of the anaphase-promoting complex/cyclosome (APC/C) ubiquitin ligase. These proteins physically interact with APC/C activators, CDC20/FZY and CDH1/FZR, in yeast two-hybrid assays. Overexpression of CDC20.1 and CCS52B/FZR3 differentially promoted ectopic endomitosis in gig1/osd1 and premature occurrence of endoreplication in uvi4. Our data suggest that GIG1/OSD1 and UVI4 may prevent an unscheduled increase in cellular ploidy by preferentially inhibiting APC/C-CDC20 and APC/C-FZR, respectively. Generation of cells with a mixed identity in gig1/osd1 further suggested that the APC/C may have an unexpected role for cell fate determination in addition to its role for proper mitotic progression.