The promoter of an apple Ypr10 gene, encoding the major allergen Mal d 1, is stress- and pathogen-inducible

Citation
H. Puhringer et al., The promoter of an apple Ypr10 gene, encoding the major allergen Mal d 1, is stress- and pathogen-inducible, PLANT SCI, 152(1), 2000, pp. 35-50
Citations number
52
Categorie Soggetti
Plant Sciences","Animal & Plant Sciences
Journal title
PLANT SCIENCE
ISSN journal
01689452 → ACNP
Volume
152
Issue
1
Year of publication
2000
Pages
35 - 50
Database
ISI
SICI code
0168-9452(20000307)152:1<35:TPOAAY>2.0.ZU;2-H
Abstract
Mal d 1 protein, constituting the major apple allergen, was classified as p athogenesis-related protein 10 (PR-10) on the basis of sequence homologies, although its induction by pathogens or stress has not been demonstrated so far. Here we report the promoter activity of a member of the apple Ypr10 g ene family and the inducibility of its gene product Mal d 1. The genomic cl one and the promoter sequence of Ypr10*a from Malus domestica have been iso lated and characterized. For gene regulation studies the promoter was trans lationally fused to the uidA reporter gene and expressed in stable transfor med Nicotiana tabacum. A total of 1.25 kb of 5' regulating sequence turned out to be necessary to direct strong beta-glucuronidase (GUS) expression. B esides the already known occurrence of Mel d 1 in ripe fruits, Ypr10 genes were found to be highly expressed only in old leaves, but can be induced in young leaves by multiple stress factors. Application of abiotic stimuli, l ike salicylic acid and reduced glutathione significantly increased both, Yp r10*a-GUS activity in transgenic tobacco and transcriptional and translatio nal expression of Mal d 1 in young apple leaves. Virus infection of the tra nsformed tobacco plants strongly induced Ypr10*a-GUS transgene expression. After treatment with fungal elicitors a clear increase in GUS activity and Mal d 1 expression was observed in young tobacco and apple leaves, respecti vely. (C) 2000 Published by Elsevier Science Ireland Ltd. All rights reserv ed.