Researchers Identify Key Plant Enzyme That Defends Against Multiple Infections
Main Category: Biology / BiochemistryArticle Date: 10 Oct 2004 - 0:00 PDT
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Scientists from the University of California, Riverside have identified one of the key enzymes that trigger programmed cell death, an important process plants undergo in fighting off bacterial, fungal or viral infections. The development holds out hope of improving crop yields, which are dependent on plants being able to fend off multiple types of pathogens.
The findings, outlined in a paper titled "VPEg Exhibits a Caspase-like Activity that Contributes to Defense Against Pathogens" were reported in the Sept. 23, online issue of Current Biology, and involve research on the key plant protein, vacuolar processing enzyme or VPEg, in Arabidopsis thaliana, or thale cress, that is required for this process.
Programmed cell death (PCD), which occurs naturally in all multi-cellular organisms, is the regulated elimination of cells that happens during the course of development, as well as in response to bacterial, fungal and viral infection. Caspases are a family of proteases, or enzymes that degrade proteins, which play an essential role in initiating and carrying out programmed cell death in animals.
Caspase-like activities have also been shown to be required for the initiation of programmed cell death in plants, but the genes controlling those activities have not been identified.
Natasha Raikhel, Director of the UCR Center for Plant Cell Biology, and her former postdoctoral researcher, Enrique Rojo, have now shown that this key plant protein contributes to defense against bacterial, fungal and viral pathogens in plants by activating programmed cell death pathways.
They have discovered that mutants lacking this protein have an increased susceptibility to these pathogens. These results have significant influence in the outcome of a diverse set of plant-pathogen interactions and suggest that this key plant protein is likely involved in a variety of processes that range from stress and defense responses to proper development during aging.
This is an important discovery because it demonstrates a previously unknown mechanism through which plants control cell death. "Programmed cell death is a universal process that all multicellular organisms must control throughout growth and development," explained Raikhel. "Since PCD plays such a central role in a wide variety of physiological processes, the VPE pathway for controlling PCD likely has a huge impact on this process in plants."
The research, funded by the National Science Foundation, was carried out from 2002-2004 in the Department of Botany and Plant Sciences and the Center for Plant Cell Biology (CEPCEB) at UC Riverside and the Universidad Autónoma de Madrid.
Besides Raikhel and Rojo, UCR co-authors of the Current Biology paper include Clay Carter, Jan Zouhar, Songqin Pan, and Hailing Jin. Co-authors from other institutions include Raquel Martin, Manuel Paneque and Jose Juan Sanchez-Serrano of the Departamento de Genética Molecular de Plantas del Centro Nacional de Biotecnología, Consejo Superior de Investigaciones Cientificas, Madrid, Spain; Frederick M Ausubel and Julia Plotnikova of the Department of Genetics at Harvard Medical School and the Department of Molecular Biology at Massachusetts General Hospital, Boston; and Barbara Baker of the Plant Gene Expression Center at UC Berkeley & the U.S. Department of Agriculture.
Additional Contacts:
Natasha Raikhel - natasha.raikhel@ucr.edu
The University of California, Riverside is a major research institution and a national center for the humanities. Key areas of research include nanotechnology, genomics, environmental studies, digital arts and sustainable growth and development. With a current undergraduate and graduate enrollment of nearly 17,000, the campus is projected to grow to 21,000 students by 2010. Located in the heart of inland Southern California, the nearly 1,200-acre, park-like campus is at the center of the region's economic development. Visit http://www.ucr.edu or call 951-UCR-NEWS for more information. Media sources are available at http://www.mediasources.ucr.edu.
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