Einset, John .
ROS Signaling is Fundamental to Chilling Stress in Arabidopsis.
Chilling stress is a key factor limiting plant survival and distribution. Both pre-harvest and post-harvest damage to plants caused by chilling stress result in enormous financial losses in agriculture every year, so new technologies and better knowledge about the nature of chilling stress could have significant economic consequences. Evidence suggests that chilling stress in Arabidopsis consists of a signal transduction pathway involving elevated levels of reactive oxygen species (ROS) as intermediates in both roots and leaves. This means that the mechanism of ROS production and its regulation are of interest. Plants exposed to a chilling stress have elevated ROS levels and inhibited root growth for up to 4 days after transfer back to optimal growing conditions. During this recovery period, ROS levels decline in root tips and in leaves. If plants are pretreated with glycine betaine (GB) prior to the chilling treatment, ROS levels do not increase during chilling and optimal growth begins as soon as plants are transferred back to normal growing conditions without a recovery period. We are interested in identifying genes involved in the chilling stress/ROS pathway and in the pathway activated by GB that blocks ROS accumulation. Using microarray and Northern technologies, we can show that GB up-regulates several genes in both roots and leaves that reinforce intracellular processes protecting cells from oxidative damage and others involved in membrane trafficking or transcription. Experiments with a knockout mutant for the membrane trafficking RabA4c provide direct evidence that this GB-activated gene is required for GB’s effects on recovery from chilling and ROS accumulation during chilling. RabA4c knockouts respond only slightly to glycine betaine, if at all, compared to wild type in relation to root growth recovery and ROS production in leaves after chilling stress. Other genes up-regulated by GB in roots include the NADPH-dependent ferric reductase (FRO2) localized to the plasmamembrane, mitochondrial catalase 2 and the cell wall peroxidase ATP3a. The FRO2 mutant frd1-1 recovers more slowly from chilling stress but, nonetheless, shows a GB response.
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1 - Norwegian University of Life Sciences, P. O. Box 5003, Aas, 1432, Norway
Presentation Type: Plant Biology Abstract
Location: Exhibit Hall (Northeast, Southwest & Southeast)/Hilton
Date: Sunday, July 8th, 2007
Time: 8:00 AM