期刊
PLANT AND CELL PHYSIOLOGY
卷 52, 期 5, 页码 922-932出版社
OXFORD UNIV PRESS
DOI: 10.1093/pcp/pcr042
关键词
Cell cycle arrest; Cyclin-dependent kinase; Elicitor; Proteasome; Synchronous culture
资金
- Japan Society for the Promotion of Science
- Ministry of Education, Science, Culture, Sports, and Technology, Japan [13039015, 17051027]
- Japan Society for the Promotion of Science [06801]
- Grants-in-Aid for Scientific Research [23380027, 23658061, 17051027, 23580068, 13039015] Funding Source: KAKEN
Induction of defense responses by pathogens or elicitors is often accompanied by growth inhibition in planta, but its molecular mechanisms are poorly understood. In this report, we characterized the molecular events that occur during cryptogein-induced cell cycle arrest at G(2) phase in synchronously cultured tobacco Bright Yellow-2 (BY-2) cells. Concomitant with the proteinaceous elicitor-induced G(2) arrest, we observed inhibition of the histone H1 kinase activity of cyclin-dependent kinases (CDKs), which correlated with a decrease in mRNA and protein levels of CDKB1. In contrast, the amount of CDKA was almost unaffected by cryptogein even at M phase. Cryptogein rapidly inhibited the expression not only of positive, e.g. A- and B-type cyclins and NtCAK, but also of negative cell cycle regulators such as WEE1, suggesting that cryptogein affects multiple targets to inactivate CDKA to induce G(2) arrest by mechanisms distinct from known checkpoint regulation. Moreover, we show that CDKB1 and cyclin proteins are also rapidly degraded by cryptogein and that the proteasome-dependent protein degradation has a crucial role in the control of cryptogein-induced hypersensitive cell death.
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