The potential importance of diversity in Eutypa lata and co-colonising fungi in explaining variation in development of grapevine dieback

1999 ◽  
Vol 103 (11) ◽  
pp. 1385-1390 ◽  
Author(s):  
J.-P. Péros ◽  
I. Jamaux-DesprÉAux ◽  
G. Berger ◽  
D. Gerba
2000 ◽  
Vol 66 (10) ◽  
pp. 4475-4480 ◽  
Author(s):  
Pascal Lecomte ◽  
Jean-Pierre Péros ◽  
Dominique Blancard ◽  
Nicolas Bastien ◽  
Christophe Délye

ABSTRACT Eutypa lata is the causal fungal agent ofEutypa dieback, a serious grapevine necrotic disease. The erratic and delayed (1 to 2 months) appearance of characteristic conidia on culture media and the presence of numerous microorganisms in decaying wood make it difficult either to identify or to detectE. lata in grapevine wood samples. We designed six pairs of PCR primers for diagnosis of E. lata. Three primer pairs were derived from ribosomal DNA internal transcribed spacer sequences, and three pairs were derived from randomly amplified polymorphic DNA fragments. The six primer pairs could be used to amplify DNAs extracted from all of the E. lata isolates tested. They did not amplify DNAs from fungi and bacteria representing more than 50 different species of microorganisms associated with grapevine. We developed a simple protocol, leading to a rapid release of DNA, that enabled us to identify E. lata from pure or mixed cultures as well as from grapevine wood samples. Identification of E. lata in wood was achieved within a few hours, instead of the several weeks required for classical cultures on agar medium. We believe that the procedure described here can be adapted to detect other microorganisms involved in woody plant diseases.


1999 ◽  
Vol 36 (5) ◽  
pp. 301-309 ◽  
Author(s):  
J.-P. Péros ◽  
G. Berger

1997 ◽  
Vol 77 (01) ◽  
pp. 001-010 ◽  
Author(s):  
Michael D P Boyle ◽  
Richard Lottenberg

SummaryIn this review the interaction between invasive human pathogens expressing plasmin(ogen) receptors and/or producing plasminogen activators with the human plasmin(ogen) system is described. Evidence is presented for multiple mechanisms by which human pathogens can acquire a surface bound form of plasmin that cannot be regulated by host serpins. The potential importance of these pathways in providing the organisms with the ability to cross tissue barriers is discussed.


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