Phytosulfokine control of growth occurs in the epidermis, is likely to be non‐cell autonomous and is dependent on brassinosteroids. (10th December 2012)

• Record Type: Journal Article
• Authors: Hartmann, Jens; Stührwohldt, Nils; Dahlke, Renate I.; Sauter, Margret
• Is Part Of: Plant journal. Volume 73:Number 4(2013:Feb.)
• Page Start: 579
• Page End: 590
• Publication Date: 2012-12-10
• Subjects: Arabidopsis thaliana -- brassinosteroid -- elongation -- epidermis -- peptide growth factor -- phytosulfokine; Plant molecular biology -- Periodicals; Plant cells and tissues -- Periodicals; Botany -- Periodicals; 580
• DOI: 10.1111/tpj.12056
• Languages: English
• ISSNs: 0960-7412

Abstract

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: PSKR1 or 35S: PSKR2 seedlings were larger, indicating that receptor abundance limits growth in planta . The preferential expression of PSKR1 in the epidermis of CER6: PSKR1 pskr1–3 pskr2–1 seedlings was sufficient to promote wild‐type growth. Moreover, in GL2:PSKR1 pskr1–3 pskr2–1 seedlings that express PSKR1 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 GL2:PSKR1 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 ), PSKR1ox12 and CER6:PSKR1–3–1 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, PSKR1ox and tpst–1 seedlings showed largely unchanged transcript levels of BR biosynthesis genes.