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Strigolactone signaling in the endodermis is sufficient to restore root responses and involves SHORT HYPOCOTYL 2 (SHY2) activity
Author(s) -
Koren Dikla,
Resnick Nathalie,
Gati Einav Mayzlish,
Belausov Eduard,
Weininger Smadar,
Kapulnik Yoram,
Koltai Hinanit
Publication year - 2013
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.12189
Subject(s) - meristem , endodermis , auxin , biology , microbiology and biotechnology , strigolactone , cytokinin , arabidopsis , arabidopsis thaliana , hypocotyl , mutant , root hair , signal transduction , lateral root , brassinosteroid , botany , genetics , gene , shoot
Summary Strigolactones ( SL s) are plant hormones and regulators of root development, including lateral root ( LR ) formation, root hair ( RH ) elongation and meristem cell number, in a MORE AXILLARY GROWTH 2 (MAX2)‐dependent way. However, whether SL signaling is acting cell‐autonomously or in a non‐cell‐autonomous way in roots is unclear. We analyzed root phenotype, hormonal responses and gene expression in multiple lines of A rabidopsis thaliana max2‐1 mutants expressing MAX 2 under various tissue‐specific promoters and shy2 mutants. The results demonstrate for the first time that expression of MAX 2 under the SCARECROW ( SCR ) promoter, expressed mainly in the root endodermis, is sufficient to confer SL sensitivity in the root for RH , LR and meristem cell number. Moreover, loss of function mutation of SHORT HYPOCOTYL 2 (SHY2), a key component in auxin and cytokinin regulation of meristem size, has been found to be insensitive to SL s in relation to LR formation and meristem cell number. Endodermal SL signaling, mediated by MAX 2, is sufficient to confer SL sensitivity in root, and SHY 2 may participate in SL signaling to regulate meristem size and LR formation. These SL signaling pathways thus may act through modulation of auxin flux in the root tip, and may indicate a root‐specific, yet non‐cell‐autonomous regulatory mode of action.