Induced chlorophyll degradation by a chlorosis toxin from Pyrenophora tritici-repentis

Citation
Se. Strelkov et al., Induced chlorophyll degradation by a chlorosis toxin from Pyrenophora tritici-repentis, CAN J PL P, 20(4), 1998, pp. 428-435
Citations number
25
Categorie Soggetti
Plant Sciences
Journal title
CANADIAN JOURNAL OF PLANT PATHOLOGY-REVUE CANADIENNE DE PHYTOPATHOLOGIE
ISSN journal
07060661 → ACNP
Volume
20
Issue
4
Year of publication
1998
Pages
428 - 435
Database
ISI
SICI code
0706-0661(199812)20:4<428:ICDBAC>2.0.ZU;2-I
Abstract
Pyrenophora tritici-repentis, causal agent of tan spot of wheat, can differ entially induce tan necrosis and extensive chlorosis in wheat. A chlorosis inducing host-specific toxin, termed Ptr ToxB (formerly Ptr chlorosis toxin ), was isolated from race 5 of P. tritici-repentis. The physiological devel opment of chlorosis in sensitive wheat was investigated using partially pur ified toxin. Treatment with the toxin had no effect on the greening of etio lated tissue, suggesting that chlorosis resulted from chlorophyll degradati on, rather than inhibition of chlorophyll synthesis. Development of chloros is was light-dependent, indicating that it may be a consequence of photoche mical bleaching. To test for the involvement of active oxygen (AO) species in photobleaching, toxin-treated tissue was floated in solutions of various AO scavengers. The compound p-benzoquinone, which quenches singlet oxygen and triplet chlorophyll, prevented the development of chlorosis, suggesting that AO species may be involved in chlorophyll degradation. High performan ce liquid chromatography (HPLC) chlorophyll degradation profiles were also consistent with photo-oxidation, Decreases in carotenoid levels were smalle r than and concurrent with the declines in chlorophyll content, indicating that toxin-induced chlorosis was not the result of a carotenoid deficiency. It appears that Ptr ToxB, directly or indirectly, inhibits photosynthesis, leading to chlorophyll photodestruction as illuminated thylakoid membranes become unable to dissipate excitation energy.