|Title||Characterization of tomato genes for resistance to Oidium neolycopersici|
|Author(s)||Seifi Abdolabad, A.R.|
|Source||University. Promotor(en): Richard Visser, co-promotor(en): Yuling Bai. - S.l. : s.n. - ISBN 9789085858799 - 140|
Laboratory of Plant Breeding
|Publication type||Dissertation, internally prepared|
|Keyword(s)||solanum lycopersicum - plantenziekteverwekkende schimmels - oidium - meeldauw - wilde verwanten - ziekteresistentie - plaagresistentie - verdedigingsmechanismen - genen - genexpressie - genetische kartering - kruisingen - plant pathogenic fungi - mildews - wild relatives - disease resistance - pest resistance - defence mechanisms - genes - gene expression - genetic mapping - crosses|
Tomato, Solanum lycopersicum, is a host for Oidium neolycopersici, the cause of powdery mildew (PM). Though cultivated tomatoes are susceptible to PM, resistance is reported in wild Solanum species. By screening wild tomato species, nine loci conferring resistance to PM have been identified, namely Ol-1, ol-2, Ol-3, Ol-4, Ol-5, Ol-6, Ol-qtl1, Ol-qtl2, andOl-qtl3. These genes are located on different chromosomes and mediate different levels of resistance by different mechanisms. In this thesis we mainly focused on the Ol genes located on chromosome 6 (Ol-1, Ol-4, Ol-5 and Ol-6) with the aim to fine-map and eventually clone these genes. In addition, we studied the contribution of different phytohormone pathways to the resistance mediated by Ol-1, ol-2, Ol-4 and Ol-qtls.
We first focused on the Ol genes on the short arm of tomato chromosome 6, Ol-4 originating from S. peruvianum LA2172 and Ol-6 with unknown origin (Chapter 2). We showed that Ol-4 and Ol-6 are homologues of the Mi-1 gene.
On the short arm of tomato chromosome 6, the Mi-1gene cluster is about 400 Kb in size and consists of several other genes besides the Mi-1 homologues. There are transport inhibitor responses-like (TIR-like) genes embedded in this cluster. Interestingly, the copy number of these TIR-like genes in the nematode-resistant tomatoes is less than that in nematode-susceptible ones (Chapter 3). Furthermore, lower expression of these TIR-like genes was observed in roots, but not in leaves, of nematode-resistant plants compared to nematode-susceptible plants. These observations prompted us to suggest and to discuss two different scenarios explaining how TIR-like genes could play a role in the plant response to root-knot nematodes.
Then, we studied the Ol-1 and Ol-5, which are located on the long arm of chromosome 6, and originated from different S. habrochaites accessions. Ol-1 is closely linked to Ol-5. With fine-mapping, we narrowed down this locus to a 73 Kb interval which contains at least 10 putative genes. Interestingly we observed an interaction between chromosome regions harboring Ol-1 and Ol-5, indicating that the interaction between Ol-1 and Ol-5 is needed to confer PM resistance. Both Ol-1 and Ol-5 trigger delayed cell death that is distinguishable from hypersensitive response (HR), the hallmark of R gene response to biotrophic pathogens. The delayed cell death associated with Ol-1 and Ol-5 resembles the autophagic PCD. We observed that Ol-1 and Ol-5 were both required for on-time and effective cell death to stop PM. If one of these two genes was not present, cell deathcould not happen or not be effective enough to stop pathogen growth.
Finally, we investigated the involvement of phytohormone pathways in PM resistance conferred by the Olgenes, including Ol-1, ol-2, Ol-4 and Ol-qtls (Chapter 5). There is overwhelming evidence implicating plant hormones in plant responses to pathogens. In this experiment we, in addition to Ol-1 and Ol-4, included other resistance loci for PM resistance in tomato. The first one is ol-2, a homologue of the barley mlo gene and derived from S. lycopersicum var cerasiforme LA1230. This gene confers resistance to PM by triggering callose deposition and, thereby, cell wall fortification. The other is Ol-qtls, a combination of three QTLs for PM resistance associated with both delayed cell deathand callose deposition. NILs carrying Ol-1, ol-2, Ol-4 and Ol-qtls, plus the background of these NILs (S. lycopersicum cv Moneymaker, MM), provided us the possibility to compare the involvement of hormonal pathways in different kinds of tomato responses. These responses include basal defense, cell wall fortification, delayed cell death,and HR. We quantified the expression of marker genes for the pathways of salicylic acid (SA), jasmonic acid (JA), abscisic acid (ABA), and ethylene (ET) over a time-course after inoculation with PM. As a complementary approach, we crossed our NILs with tomato mutants for JA, ET and ABA. Our results suggested that Ol-4-mediated resistance probably relies on the SA pathway. Ol-1 and Ol-qtls require ET to promote the delayed cell deathfor PM resistance. JA deficiency can compromise resistance mediated by ol-2. Our results also suggested that ABA is required for those interactions demanding callose deposition, resistance associated with ol-2 and Ol-qtls. These results present a nice example of the involvement of different phytohormones in different phases of resistance against PM in tomato. Altogether, this thesis describes different tomato resistance mechanisms triggered by different resistance genes in the same pathosystem, underscoring the plant ability to adopt diverse molecular mechanisms to defense itself against intruders.