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Transcriptional repression of the APC/C activator CCS52A1 promotes active termination of cell growth
Article first published online: 9 NOV 2012
Copyright © 2012 European Molecular Biology Organization
The EMBO Journal
Volume 31, Issue 24, pages 4488–4501, December 12, 2012
How to Cite
Breuer, C., Morohashi, K., Kawamura, A., Takahashi, N., Ishida, T., Umeda, M., Grotewold, E. and Sugimoto, K. (2012), Transcriptional repression of the APC/C activator CCS52A1 promotes active termination of cell growth. The EMBO Journal, 31: 4488–4501. doi: 10.1038/emboj.2012.294
- Issue published online: 12 DEC 2012
- Article first published online: 9 NOV 2012
- Manuscript Accepted: 2 OCT 2012
- Manuscript Received: 31 JUL 2012
- cell growth;
- trihelix transcription factor
Spatial and temporal control of cell growth is central for the morphogenesis of multicellular organisms. For some cell types that undergo extensive post-mitotic cell growth, such as neurons and hair cells, orchestrating the extent of post-mitotic cell growth with development is vital for their physiology and function. Previous studies suggested that the extent of cell growth is linked with an increase in ploidy by endoreduplication but how developmental signals control endocycling and cell growth is not understood in both animals and plants. In this study we show that a trihelix transcription factor, GT2-LIKE 1 (GTL1), actively terminates ploidy-dependent cell growth and its developmentally regulated expression is one of the key determinants of cell size in Arabidopsis leaf hair cells (trichomes). Through genome-wide chromatin-binding studies (ChIP-chip) coupled with transcriptional profiling, we further demonstrate that GTL1 directly represses the transcription of CDH1/FZR/CCS52, an activator of the anaphase-promoting complex/cyclosome (APC/C), to stop the endocycle progression and ploidy-dependent cell growth. Thus, our findings uncover a previously uncharacterised key molecular link between developmental programming and cell-size control, highlighting the central role of APC/C in post-mitotic cell growth.