|THOMPSON, ASUNTA - North Dakota State University|
Submitted to: Journal of Plant Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/16/2011
Publication Date: 1/27/2012
Citation: Neubauer, J., Lulai, E.C., Thompson, A.L., Suttle, J.C., Bolton, M.D. 2012. Wounding coordinately induces cell wall protein, cell cycle and pectin methyl esterase genes involved in tuber closing layer and wound periderm development. Journal of Plant Physiology. 169:584-595.
Interpretive Summary: • Potato tubers (Solanum tuberosum L.) are wounded upon harvest, handling and seed cutting. These wounds must heal quickly to avoid costly infection and deterioration of food quality. Mechanisms that may hasten/regulate these healing processes are of great importance. However, little is known about the coordinate induction of genes that may be associated with or mark major wound-healing events. In this study, the occurrence of critical wound-healing events were determined in coordination with wound-induced expression profiles of genes thought to be involved in cell division and cell wall construction as part of wound repair. The study was conducted using two diverse potato genotypes and two harvests (NDTX4271-5R and Russet Burbank tubers; 2008 and 2009 harvests). By 5 days after wounding, tubers had begun to repair the damaged area by chemically modifying the outer surface of wounded cells and by forming a layer of cells that begin to divide and close the wounded area. The expression of genes involved in these early events leading to cell division was stimulated within one day of wounding and this increase coincided with wound-induced cell division. Additional genes involved in cell wall modification that follows cell division and is an essential component of the wounding healing process were expressed one to five days after wounding. A final group of genes that are thought to increase cell wall strength was induced late in the wound healing process. The identification of these genes provides important new information about the wound healing process of tubers and may lead to the development of new methods to monitor and speed this agriculturally important process thereby greatly reducing postharvest losses and the financial burden on growers.
Technical Abstract: Potato (Solanum tuberosum L.) is the world’s fourth largest food crop and large financial losses are incurred each year from wound and bruise related injuries. However, little is known about the coordinate induction of genes that may be associated with or mark major wound-healing events. In this study, wound-healing events were determined in coordination with wound-induced expression profiles of selected cell cycle, cell wall protein, and pectin methyl esterase genes using two diverse potato genotypes and two harvests (NDTX4271-5R and Russet Burbank tubers; 2008 and 2009 harvests). By 5 d after wounding, the closing layer and a nascent phellogen had formed. Phellogen cell divisions generated phellem cell layers until cessation of cell division at 28 d after wounding for both genotypes and harvests. Cell cycle genes encoding epidermal growth factor binding protein (StEBP), cyclin-dependent kinase B (StCDKB) and cyclin-dependent kinase regulatory subunit (StCKS1At) were induced by 1 d after wounding; expression profiles of these genes coordinated with related phellogen formation and the induction and cessation of phellem cell formation. Genes encoding the structural cell wall proteins extensin (StExt1) and extensin-like (StExtlk) were dramatically up-regulated by 1 d to 5 d after wounding, suggesting involvement with closing layer formation and later phellem cell layer formation. The coordinate induction and expression profile of StTLRP, a gene encoding a cell wall strengthening “tyrosine-and lysine-rich protein,” suggested a role in the formation of the closing layer followed by phellem cell generation and lastly cell wall thickening in non-meristematic phellogen cells. Wounding up-regulated pectin methyl esterase genes (StPME and StPrePME); StPME expression increased during closing layer and phellem cell formation, whereas maximum expression of StPrePME expression occurred at 5 d to 14 d after wounding, implicating involvement in later modifications for closing layer and phellem cell formation. Collectively, these results indicate that the genes monitored were wound-inducible and their expression profiles markedly coordinated with closing layer formation and the indices for meristematic activity of the phellogen layer during wound periderm development; results were influenced by harvest but not genotype. Importantly, StTLRP was the only gene examined that may be involved in phellogen cell wall strengthening or thickening after cessation of cell division.