|TALBOT, MARK - U OF NEWCASTLE/AUSTRALIA
|OFFLER, CHRISTINA - U OF NEWCASTLE/AUSTRALIA
|MCCURDY, DAVID - U OF NEWCASTLE/AUSTRALIA
Submitted to: Plant and Cell Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/25/2006
Publication Date: 1/26/2007
Citation: Vaughn, K.C., Talbot, M.J., Offler, C.E., Mccurdy, D.W. 2007. Wall ingrowths in epidermal transfer cell of Vica faba Cotyledons are modified primary walls marked by localized accumulations of Arabinogalactan proteins. Journal of Plant Cell Physiology 48(1):159-168.
Interpretive Summary: A number of herbicides affect cell wall formation but studies are hampered in that plant cell walls have existing cell walls so that affects of inhibition may not be studied. In this study, we took advantage of a novel system where cell walls are made de novo to monitor the effects of two herbicides and another potential cell wall inhibitor. Using this system we could document 90% reduction in new cell wall formation with either herbicide and a 50% reduction with another inhibitor. This is the first direct proof of the herbicidal effects of these two compounds on de novo wall formation.
Technical Abstract: Abaxial epidermal cells of cotyledons of Vicia faba may be induced to produce labyrinthine wall ingrowths under the influence of external carbohydrate source so as to facilitate uptake of this external carbon. The induction of transfer cell type morphology allows us to a unique opportunity to monitor de novo wall formation. Using affinity probes and antibodies specific to polysaccharides, we probed thin sections of the mature epidermal transfer cells to determine the distribution of polysaccharides and glycoproteins in these structures. The outer walls of the transfer cell can be divided into three portions that vary in composition: the pre-existing primary wall, the inner more electron-opaque wall ingrowth areas, and the outer electron translucent wall areas. The primary wall reacts strongly with the esterified pectin monoclonal, xyloglucan monoclonal and polyclonals, RG-1 side chain monoclonals, and the cellulase-gold affinity probe. A very small layer at the cuticle/ wall interface reacts strongly with de-esterified pectin antibodies as does the middle lamellae. The electron translucent areas of the wall ingrowth (WI) display a similar labeling pattern to the primary wall with all of the antibodies. The outer electron transparent layer of the wall ingrowth reacts strongly with anti-callose monoclonal and polyclonal antibodies but shows no reaction for pectin or xyloglucan antibodies or the cellulase-gold affinity probe. The plasmamembrane-wall interface is labeled strongly with anti- arabinogalatan protein (AGP) antibodies, with some of the AGP antibodies also labeling the electron transparent zone as well. Nascent WI's are labeled with AGPs (with ratios up to 80: 1 compared to the plasma membrane) but not anti-callose, however, indicating that the initiation of WI's is controlled by AGPs. WI formation was inhibited by the cellulose biosynthesis inhibitor herbicides, dichobenil and isoxaben, and the beta 'Yariv reagent, an AGP disrupter. The presence of very strong labeling of callose and AGP in the electron translucent areas of the ingrowth indicates that the spreading influence of callose and the direction of new wall synthesis by AGPs is responsible for the production of these labyrinthine wall formations.