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Background   Verticillium longisporum  is a soil-borne vascular pathogen infecting cruciferous hosts such as oilseed rape. Quantitative disease resistance (QDR) is the major control means, but its molecular basis is poorly understood so far. Quantitative trait locus (QTL) mapping was performed using a new (Bur×L er ) recombinant inbred line (RIL) population of  Arabidopsis thaliana . Phytohormone measurements and analyses in defined mutants and near-isogenic lines (NILs) were used to identify genes and signalling pathways that underlie different resistance QTL.    Results  QTL for resistance to  V. longisporum -induced stunting, systemic colonization by the fungus and for  V. longisporum -induced chlorosis were identified. Stunting resistance QTL were contributed by both parents. The strongest stunting resistance QTL was shown to be identical with  Erecta . A functional  Erecta  pathway, which was present in Bur, conferred partial resistance to  V. longisporum -induced stunting. Bur showed severe stunting susceptibility in winter. Three stunting resistance QTL of L er  origin, two co-localising with wall-associated kinase-like ( Wakl ) - genes, were detected in winter. Furthermore, Bur showed a much stronger induction of salicylic acid (SA) by  V. longisporum  than L er . Systemic colonization was controlled independently of stunting. The  vec1  QTL on chromosome 2 had the strongest effect on systemic colonization. The same chromosomal region controlled the level of abscisic acid (ABA) and jasmonic acid (JA) in response to  V. longisporum : The level of ABA was higher in colonization-susceptible L er  than in colonization-resistant Bur after  V. longisporum  infection. JA was down-regulated in Bur after infection, but not in L er . These differences were also demonstrated in NILs, varying only in the region containing  vec1 . All phytohormone responses were shown to be independent of  Erecta .    Conclusions  Signalling systems with a hitherto unknown role in the QDR of  A. thaliana  against  V. longisporum  were identified:  Erecta  mediated resistance against  V. longisporum -induced stunting. Independent of  Erecta , stunting was caused in a light-dependent manner with possible participation of SA and  Wakl  genes. ABA and JA showed a genotype-specific response that corresponded with systemic colonization by the fungus. Understanding the biological basis of phenotypic variation in  A. thaliana  with respect to  V. longisporum  resistance will provide new approaches for implementing durable resistance in cruciferous crops.

ERECTA, salicylic acid, abscisic acid, and jasmonic acid modulate quantitative disease resistance of Arabidopsis thaliana to Verticillium longisporum