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Transcriptional control of ROS homeostasis by KUODA1 regulates cell expansion during leaf development
The final size of an organism, or of single organs within an organism, depends on an intricate coordination of cell proliferation and cell expansion. Although organism size is of fundamental importance, the molecular and genetic mechanisms that control it remain far from understood. Here we identify...
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Published in: | Nature communications 2014-05, Vol.5 (1), p.3767-3767, Article 3767 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | The final size of an organism, or of single organs within an organism, depends on an intricate coordination of cell proliferation and cell expansion. Although organism size is of fundamental importance, the molecular and genetic mechanisms that control it remain far from understood. Here we identify a transcription factor, KUODA1 (KUA1), which specifically controls cell expansion during leaf development in
Arabidopsis thaliana
. We show that
KUA1
expression is circadian regulated and depends on an intact clock. Furthermore, KUA1 directly represses the expression of a set of genes encoding for peroxidases that control reactive oxygen species (ROS) homeostasis in the apoplast. Disruption of
KUA1
results in increased peroxidase activity and smaller leaf cells. Chemical or genetic interference with the ROS balance or peroxidase activity affects cell size in a manner consistent with the identified KUA1 function. Thus, KUA1 modulates leaf cell expansion and final organ size by controlling ROS homeostasis.
During plant development, organ size is controlled by cell proliferation and expansion, but the molecular mechanisms involved are unclear. Here, Lu
et al.
show that leaf cell expansion is controlled by the KUA1 transcription factor that acts in a circadian manner and modulates the expression of genes encoding cell wall-localized peroxidases. |
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ISSN: | 2041-1723 2041-1723 |
DOI: | 10.1038/ncomms4767 |