Oligandrin. A proteinaceous molecule produced by the mycoparasite Pythium oligandrum induces resistance to Phytophthora parasitica infection in tomato plants

Citation
K. Picard et al., Oligandrin. A proteinaceous molecule produced by the mycoparasite Pythium oligandrum induces resistance to Phytophthora parasitica infection in tomato plants, PLANT PHYSL, 124(1), 2000, pp. 379-395
Citations number
47
Categorie Soggetti
Plant Sciences","Animal & Plant Sciences
Journal title
PLANT PHYSIOLOGY
ISSN journal
00320889 → ACNP
Volume
124
Issue
1
Year of publication
2000
Pages
379 - 395
Database
ISI
SICI code
0032-0889(200009)124:1<379:OAPMPB>2.0.ZU;2-U
Abstract
A low-molecular weight protein, termed oligandrin, was purified to homogene ity from the culture filtrate of the mycoparasitic fungus Pythium oligandru m. When applied to decapitated tomato (Lycopersicon esculentum Mill. var. P risca) plants, this protein displayed the ability to induce plant defense r eactions that contributed to restrict stem cell invasion by the pathogenic fungus Phytophthora parasitica. According to its N-terminal sequence, low-m olecular weight, acidic isoelectric Feint, ultraviolet spectrum, and migrat ion profile, the P. oligandrum-produced oligandrin was found to share some similarities with several elicitins from other Phytophthora spp. and Pythiu m spp. However, oligandrin did not induce hypersensitive reactions. A signi ficant decrease in disease incidence was monitored in oligandrin-treated pl ants as compared with water-treated plants. Ultrastructural investigations of the infected tomato stem tissues from non-treated plants showed a rapid colonization of all tissues associated with a marked host cell disorganizat ion. In stems from oligandrin-treated plants, restriction of fungal growth to the outermost tissues and decrease in pathogen viability were the main f eatures of the host-pathogen interaction. Invading fungal cells were marked ly damaged at a time when the cellulose component of their cell walls was q uite well preserved. Host reactions included the plugging of intercellular spaces as well as the occasional formation of wall appositions at sites of potential pathogen entry. In addition, pathogen ingress in the epidermis wa s associated with the deposition of an electron-opaque material in most inv aded intercellular spaces. This material, lining the primary walls, usually extended toward the inside to form deposits that frequently interacted wit h the wall of invading hyphae. In the absence of fungal challenge, host rea ctions were not detected.