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Phytosulfokine control of growth occurs in the epidermis, is likely to be non‐cell autonomous and is dependent on brassinosteroids
Author(s) -
Hartmann Jens,
Stührwohldt Nils,
Dahlke Renate I.,
Sauter Margret
Publication year - 2013
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/tpj.12056
Subject(s) - brassinosteroid , epidermis (zoology) , biology , arabidopsis , wild type , microbiology and biotechnology , autocrine signalling , cell growth , endodermis , receptor , mutant , gene , botany , genetics , anatomy
Summary Phytosulfokine ( PSK ) is a secreted disulfated pentapeptide that controls root and shoot growth. The ubiquitous expression of PSK precursor and of the LRR receptor kinase genes in Arabidopsis raised the question of whether PSK acts as an autocrine growth factor in planta . Expression of PSKR1 under the control of tissue‐ and cell type‐specific promoters in a receptor null background strongly suggests that PSK is a non‐cell autonomous signal that controls growth through localized activity in the epidermis. pskr1–3 pskr2–1 seedlings had shorter roots and hypocotyls than the wild type, whereas 35S: PSKR 1 or 35S: PSKR2 seedlings were larger, indicating that receptor abundance limits growth in planta . The preferential expression of PSKR 1 in the epidermis of CER 6: PSKR1 pskr1–3 pskr2–1 seedlings was sufficient to promote wild‐type growth. Moreover, in GL 2: PSKR 1 pskr1–3 pskr2–1 seedlings that express PSKR 1 in atrichoblasts of the root epidermis, root growth was restored to wild‐type levels. In pskr1–3 pskr2–1 seedlings, trichoblasts and atrichoblasts were shorter than in the wild type. Trichoblasts of GL 2: PSKR 1 pskr1–3 pskr2–1 seedlings, which are unable to sense PSK , nonetheless had acquired wild‐type length, suggesting that PSK acts as a non‐cell autonomous signal. Inhibition of brassinosteroid ( BR ) biosynthesis with brassinazole ( BZ ) caused a loss of responsiveness to PSK in wild‐type, tpst–1 ( tyrosylprotein sulfotransferase–1 ), PSKR 1ox12 and CER 6: PSKR 1–3–1 seedlings, as did the genetic knock‐out of BR synthesis in det2–1 and of BR perception in bri1–9 , suggesting that BR mediates PSK ‐dependent growth. Quantitative PCR analysis of BR ‐related genes in wild‐type, pskr1–3 pskr2–1 , PSKR 1ox and tpst–1 seedlings showed largely unchanged transcript levels of BR biosynthesis genes.