Temperature and leaf wetness duration affect phenotypic expression of Rlm6-mediated resistance to Leptosphaeria maculans in Brassica napus

Abstract

Near-isogenic Brassica napus lines carrying/lacking resistance gene Rlm6 were used to investigate the effects of temperature and leaf wetness duration on phenotypic expression of Rlm6-mediated resistance. Leaves were inoculated with ascospores or conidia of Leptosphaeria maculans carrying the effector gene AvrLm6. Incubation period to the onset of lesion development, number of lesions and lesion diameter were assessed. Symptomless growth of L. maculans from leaf lesions to stems was investigated using a green fluorescent protein (GFP) expressing isolate carrying AvrLm6. L. maculans produced large grey lesions on Darmor (lacking Rlm6) at 5-25 degrees C and DarmorMX (carrying Rlm6) at 25 degrees C, but small dark spots and 'green islands' on DarmorMX at 5-20 degrees C. With increasing temperature/wetness duration, numbers of lesions/spots generally increased. GFP-expressing L. maculans grew from leaf lesions down leaf petioles to stems on DarmorMX at 25 degrees C but not at 15 degrees C. We conclude that temperature and leaf wetness duration affect the phenotypic expression of Rlm6-mediated resistance in leaves and subsequent L. maculans spread down petioles to produce stem cankers.

Effector-triggered defence against apoplastic fungal pathogens

“…A microscopic reaction involving cell death occurs 8 days after leaf inoculation of B. napus cv. DarmorMX (carrying the resistance gene Rlm6 ) with ascospores of a L. maculans isolate carrying the corresponding AvrLm6 gene [32]. However, there has been subcellular evidence of necrosis occurring by 6 days after infiltration of oilseed rape cotyledons with L. maculans conidia [33].…”

“…An AvrLm1 -dependent increase in expression of the pathogenesis-related (PR) gene PR1 was detected at 5 days after infiltration with conidia, at the same time as an increase in salicylic acid production [33]. These host defence responses against L. maculans do not eliminate the pathogen, which can be re-isolated from resistant host tissue and cultured [32].…”

“…(E2) ETD against C. fulvum growing in the apoplast of a tomato was associated with cell-wall enforcement (black arrow) without visible cell death early after inoculation (3 dpi) but (F2) no cell-wall enforcement had taken place on susceptible tomato plants at 3 dpi with the virulent C. fulvum race (H: pathogen hyphae, white arrow) [75]. (G1) ETD triggered by the Leptosphaeria maculans (phoma leaf spot) AvrLm6 effector when it was recognised by the Rlm6 receptor on the resistant oilseed rape cultivar DarmorMX did not involve symptom development by 11 dpi with ascospores (without wounding) [32]. (G2) Small dark spots (black arrows) and green islands (white arrows) were observed on DarmorMX 18 dpi when the leaf started to senesce.…”

“…(L) No obvious necrosis was induced in the recessive tsn1 line BR34 by 5 days post infiltration with the same ToxA isoform [77]. Modified, with permission, from [8] (A2, A3, A4, B1, B2, B3), [11] (C2, D2), [75] (E2, F2), [32] (G1, G2, G3, H3, H4), [76] (H1, H2), and [77] (K,L). C1, D1 provided by Wolfgang Knogge (Leibniz Institute of Plant Biochemistry, Germany); D3 by Kevin King and Jean Devonshire (Rothamsted Research, UK); and I, J1, and J2 by Vivianne Vleeshouwers (Wageningen University, The Netherlands).…”

Assessing Quantitative Resistance against Leptosphaeria maculans (Phoma Stem Canker) in Brassica napus (Oilseed Rape) in Young Plants

“…Conidia (asexual spores), produced in pycnidia (asexual fruiting bodies) on leaf lesions and spread by rain-splash, can cause secondary leaf infections [25]. From leaf lesions, L. maculans grows symptomlessly along the leaf vein/petiole to reach the stem where, in spring/summer (April-July), it causes stem cankers that result in yield losses [9], [18].…”