DELLA Signaling Mediates Stress-Induced Cell Differentiation in Arabidopsis Leaves through Modulation of Anaphase-Promoting Complex/Cyclosome Activity

被引:67
作者
Claeys, Hannes [1 ,2 ]
Skirycz, Aleksandra [1 ,2 ]
Maleux, Katrien [1 ,2 ]
Inze, Dirk [1 ,2 ]
机构
[1] VIB, Dept Plant Syst Biol, B-9052 Ghent, Belgium
[2] Univ Ghent, Dept Plant Biotechnol & Bioinformat, B-9052 Ghent, Belgium
关键词
GIBBERELLIN-INDUCED DEGRADATION; LEAF DEVELOPMENT; SEED-GERMINATION; KINASE INHIBITOR; ENDOCYCLE ONSET; PROTEIN-KINASE; WATER-DEFICIT; THALIANA; GROWTH; CYCLE;
D O I
10.1104/pp.112.195032
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Drought is responsible for considerable yield losses in agriculture due to its detrimental effects on growth. Drought responses have been extensively studied, but mostly on the level of complete plants or mature tissues. However, stress responses were shown to be highly tissue and developmental stage specific, and dividing tissues have developed unique mechanisms to respond to stress. Previously, we studied the effects of osmotic stress on dividing leaf cells in Arabidopsis (Arabidopsis thaliana) and found that stress causes early mitotic exit, in which cells end their mitotic division and start endoreduplication earlier. In this study, we analyzed this phenomenon in more detail. Osmotic stress induces changes in gibberellin metabolism, resulting in the stabilization of DELLAs, which are responsible for mitotic exit and earlier onset of endoreduplication. Consequently, this response is absent in mutants with altered gibberellin levels or DELLA activity. Mitotic exit and onset of endoreduplication do not correlate with an up-regulation of known cell cycle inhibitors but are the result of reduced levels of DP-E2F-LIKE1/E2Fe and UV-B-INSENSITIVE4, both inhibitors of the developmental transition from mitosis to endoreduplication by modulating anaphase-promoting complex/cyclosome activity, which are down-regulated rapidly after DELLA stabilization. This work fits into an emerging view of DELLAs as regulators of cell division by regulating the transition to endoreduplication and differentiation.
引用
收藏
页码:739 / +
页数:12
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