Cytokinin signaling regulates pavement cell morphogenesis in Arabidopsis Journal Article

Author(s): Li, Hongjiang; Xu, Tongda; Lin, Deshu; Wen, Mingzhang; Xie, Mingtang; Duclercq, Jérôme; Bielach, Agnieszka; Kim, Jungmook; Reddy, G Venugopala; Zuo, Jianru; Benková, Eva; Friml, Jiří; Guo, Hongwei; Yang, Zhenbiao
Article Title: Cytokinin signaling regulates pavement cell morphogenesis in Arabidopsis
Abstract: The puzzle piece-shaped Arabidopsis leaf pavement cells (PCs) with interdigitated lobes and indents is a good model system to investigate the mechanisms that coordinate cell polarity and shape formation within a tissue. Auxin has been shown to coordinate the interdigitation by activating ROP GTPase-dependent signaling pathways. To identify additional components or mechanisms, we screened for mutants with abnormal PC morphogenesis and found that cytokinin signaling regulates the PC interdigitation pattern. Reduction in cytokinin accumulation and defects in cytokinin signaling (such as in ARR7-over-expressing lines, the ahk3cre1 cytokinin receptor mutant, and the ahp12345 cytokinin signaling mutant) enhanced PC interdigitation, whereas over-production of cytokinin and over-activation of cytokinin signaling in an ARR20 over-expression line delayed or abolished PC interdigitation throughout the cotyledon. Genetic and biochemical analyses suggest that cytokinin signaling acts upstream of ROPs to suppress the formation of interdigitated pattern. Our results provide novel mechanistic understanding of the pathways controlling PC shape and uncover a new role for cytokinin signaling in cell morphogenesis.
Keywords: Arabidopsis; Cytokinin; cell morphogenesis; pavement cells
Journal Title: Cell Research
Volume: 23
Issue 2
ISSN: 1748-7838
Publisher: Nature Publishing Group  
Date Published: 2013-02-01
Start Page: 290
End Page: 299
DOI: 10.1038/cr.2012.146
Notes: is work was supported by grants from the US National Institute of General Medical Sciences (GM081451 and GM081451-03S2) to ZY. We thank National Science Foundation grant (IOS-1147250) to GVR and MX. HL and DL were partially supported by the Chinese Scholarship Council.
Open access: yes (repository)