Sammanfattning

Leptosphaeria maculans causes blackleg disease, and resistance to this fungal pathogen is an important trait in the breeding of oil-seed rape. A better comprehension of the role of the myrosinase-glucosinolate system in this context is of great value. The present study is the first to address effects on multiple components of this complex system, including concentrations of individual glucosinolates, product formation, myrosinase isoform distribution and activity, and levels of myrosinase binding proteins during the infection process. One resistant B. napus cultivar (Maluka) and one susceptible cultivar (Westar) were compared in the investigation. Our results show that the two cultivars had the same histological distribution, isoform expression, and activity of the myrosinase enzymes. The glucosinolate levels were also similar, with the exception of glucobrassicin and neoglucobrassicin, which were significantly lower in the resistant cultivar at 11 days post-infection. Growth of the fungus on the plant tissues did not alter glucosinolate levels, suggesting that L. maculans does not degrade these compounds. When the plants were starved of sulphur, and thereby depleted of glucosinolates, no increased susceptibility was observed. Hence, we suggest that the myrosinase-glucosinolate system does not determine the outcome of the interaction between B. napus and L. maculans.

Publicerad i

Molecular Plant Pathology
2001, Volym: 2, nummer: 5, sidor: 281-286

SLU författare

• Andreasson, Erik

  • Københavns Universitet
  • Sveriges lantbruksuniversitet, Sveriges lantbruksuniversitet
    

• Dixelius, Christina

  • Sveriges lantbruksuniversitet, Sveriges lantbruksuniversitet
    

• Rask, Lars

  • Sveriges lantbruksuniversitet, Sveriges lantbruksuniversitet
    
  • Uppsala universitet

• Meijer, Johan

  • Sveriges lantbruksuniversitet, Sveriges lantbruksuniversitet
    

UKÄ forskningsämne

Växtbioteknologi


Publikationens identifierare

DOI: https://doi.org/10.1046/j.1464-6722.2001.00076.x

Permanent länk till denna sida (URI)

https://res.slu.se/id/publ/39073