Premium
Gh WIP 2, a WIP zinc finger protein, suppresses cell expansion in Gerbera hybrida by mediating crosstalk between gibberellin, abscisic acid, and auxin
Author(s) -
Ren Guiping,
Li Lingfei,
Huang Yuhua,
Wang Yaqin,
Zhang Wenbin,
Zheng Rouyan,
Zhong Chunmei,
Wang Xiaojing
Publication year - 2018
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/nph.15175
Subject(s) - auxin , biology , crosstalk , gibberellin , abscisic acid , microbiology and biotechnology , repressor , arabidopsis , agamous , bryopsida , zinc finger , transcription factor , gene , genetics , mutant , physics , optics
Summary Cell expansion is a key determinant for the final size and shape of plant organ, and is regulated by various phytohormones. Zinc finger proteins ( ZFP s) consist of a superfamily involved in multiple aspects of organ morphogenesis. However, little is known about WIP ‐type ZFP function in phytohormone‐mediated organ growth. Using reverse genetics, RNA ‐seq and phytohormone quantification, we elucidated the role of a new WIP ‐type ZFP from Gerbera hybrida , Gh WIP 2, in controlling organ growth via regulation of cell expansion. Gh WIP 2 localizes to the nucleus and acts as a transcriptional repressor. Constitutive overexpression of Gh WIP 2 (Gh WIP 2 OE ) in both Gerbera and Arabidopsis thaliana caused major developmental defects associated with cell expansion, including dwarfism, short petals, scapes, and petioles. Furthermore, Gh WIP 2 OE plants were hypersensitive to GA , but not to ABA , and showed a reduction in endogenous GA and auxin, but not ABA concentrations. Consistent with these observations, RNA ‐seq analysis revealed that genes involved in GA and auxin signaling were down‐regulated, while those involved in ABA signaling were up‐regulated in Gh WIP 2 OE plants. Our findings suggest that Gh WIP 2 acts as a transcriptional repressor, suppressing cell expansion during organ growth by modulating crosstalk between GA , ABA , and auxin.