Research has shown that the tomato's genetic resistance to the fungal disease powdery mildew is dependent on monogenic and polygenic resistance. Many resistance genes have been localised on tomato chromosome six. In addition, the resistance mechanisms and the specificity of the resistance genes in general have been shown to be very diverse. These findings are contained in the research carried out by Yuling Bai at Wageningen University for her thesis: 'The genetics and mechanisms of resistance to tomato powdery mildew in Lycopersicon species'. Her work provides important new information for growers in their fight against this major fungal disease.
Powdery mildew is a disease caused by the fungus Oidium neolycopersici,which was first identified in Dutch tomato cultivation in 1986. Since thisdate the fungus has spread worldwide and been the cause of major problems.Little is known about O. neolycopersici and, with the exception ofa few varieties of tomato recently brought onto the market, virtually alltomato varieties are susceptible to the fungus. As a result, chemical pesticidesare used to combat its effects. The research by Bai into the mechanisms andthe genetic basis of resistance to O. neolycopersici offers freshleads for the development of new tomato varieties with sustainable resistance.
Bai succeeded in crossing resistance genes identified in wild tomatospeciesinto nearly isogenic lines (NILs) from the - by nature susceptible - tomatocultivar “Money Maker”. These plant lines are almost identicalgenetically, with the exception of the resistance genes in question.
Using molecular markers and resistance tests, Bai discovered five dominantmonogenic resistant genes, all of which are located on chromosome six. Earlierresearch has shown that chromosome six is a hot spot of resistant genes, includingresistances against the leaf mould disease, viruses, nematodes, lice and whitefly.In addition, Bai analysed the quantitative resistance in the wild tomato varietyL. parviflorum and found that the resistance was defined by at leastthree genetic loci (Quantitative Trait Loci/QTL). One of these QTL was alsolocalised on chromosome six, linked to the monogenic resistance genes.
The fact that many resistance genes are localised on chromosome 6 is interestingfrom an evolutionary perspective, since many resistances involve the gene-for-geneinteraction. In such an interaction, a fungal avirulence factor is recognizedby a plant resistance protein, which triggers the resistance response. Whenthe fungal DNA encoding the avirulence factor is 'coincidentally' changedby small mistakes during the cell division, the plant no longer recognises(the avirulence factors of) the fungus and no resistance reaction takes place.
This means the plant is no longer resistant to that fungal isolate. Becausethe plant's resistance genes are arranged in tandem arrays, new varietiesof the genes can arise via incorrect chromosome pairing and recombinationduring the sexual cell division. This can lead to renewed recognition of thefungal isolate.
Various isolates of the fungus are present in the different countries wherepowdery mildew appears. In order to find out whether certain resistance genescan specifically work against certain varieties of the fungus, seeds of the"resistant" tomato NILs were sent to Florida and various countriesin Europe. These plants were then exposed to the local fungus. In the CzechRepublic, a tomato line with a specific monogenic resistance was susceptibleto the fungus, which shows that the resistance is race specific and can beovercome by the fungus.
Bai's findings have provided greater insight into the interaction betweentomato plants and O. neolycopersici. As a consequence, sustainableresistance, which the fungus cannot overcome or if so only with difficulty,is now within reach.
NOTE FOR EDITORS
Yuling Bai will defend her thesis: ‘The genetics and mechanisms of resistanceto tomato powdery mildew in Lycopersicon species’ on Wednesday 29 Septemberat 13.30 in the Wageningen University aula: Gen. Foulkesweg 1a, Wageningen.
For more information and illustrations of affected plants: Edwin Luijks,tel. +31 (0) 317 48 39 15, email: Edwin.Luijks@wur.nl.Questions on the content should be addressed to Guusje A. Bonnema, email:Guusje.Bonnema@wur.nl or Y. Bai,email: Bai.Yuling@wur.nl.