Abstract
BACKGROUND
The phoma stem canker pathogen Leptosphaeria maculans is one of the most widespread and devastating pathogens of oilseed rape (Brassica napus) in the world. Pathogen colonization is stopped by an interaction of a pathogen Avr effector gene with the corresponding host resistance (R) gene. While molecular mechanisms of this gene-for-gene interaction are being elucidated, understanding of effector function remains limited. The purpose of this study was to determine the action of L. maculans effector (AvrLm) genes on incompatible interactions triggered by B. napus noncorresponding R (Rlm) genes. Specifically, effects of AvrLm4-7 and AvrLm1 on Rlm7-mediated resistance were studied.
RESULTS
Although there was no major effect on symptom expression, induction of defence genes (e.g. PR1) and accumulation of reactive oxygen species was reduced when B. napus cv. Excel carrying Rlm7 was challenged with a L. maculans isolate containing AvrLm1 and a point mutation in AvrLm4-7 (AvrLm1, avrLm4-AvrLm7) compared to an isolate lacking AvrLm1 (avrLm1, AvrLm4-AvrLm7). AvrLm7-containing isolates, isogenic for presence or absence of AvrLm1, elicited similar symptoms on hosts with or without Rlm7, confirming results obtained with more genetically diverse isolates.
CONCLUSION
Careful phenotypic examination of isogenic L. maculans isolates and B. napus introgression lines demonstrated a lack of effect of AvrLm1 on Rlm7-mediated resistance despite an apparent alteration of the Rlm7-dependent defence response using more diverse fungal isolates with differences in AvrLm1 and AvrLm4. As deployment of Rlm7 resistance in crop cultivars increases, other effectors need to be monitored because they may alter the predominance of AvrLm7. © 2023 The Authors. Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.
The phoma stem canker pathogen Leptosphaeria maculans is one of the most widespread and devastating pathogens of oilseed rape (Brassica napus) in the world. Pathogen colonization is stopped by an interaction of a pathogen Avr effector gene with the corresponding host resistance (R) gene. While molecular mechanisms of this gene-for-gene interaction are being elucidated, understanding of effector function remains limited. The purpose of this study was to determine the action of L. maculans effector (AvrLm) genes on incompatible interactions triggered by B. napus noncorresponding R (Rlm) genes. Specifically, effects of AvrLm4-7 and AvrLm1 on Rlm7-mediated resistance were studied.
RESULTS
Although there was no major effect on symptom expression, induction of defence genes (e.g. PR1) and accumulation of reactive oxygen species was reduced when B. napus cv. Excel carrying Rlm7 was challenged with a L. maculans isolate containing AvrLm1 and a point mutation in AvrLm4-7 (AvrLm1, avrLm4-AvrLm7) compared to an isolate lacking AvrLm1 (avrLm1, AvrLm4-AvrLm7). AvrLm7-containing isolates, isogenic for presence or absence of AvrLm1, elicited similar symptoms on hosts with or without Rlm7, confirming results obtained with more genetically diverse isolates.
CONCLUSION
Careful phenotypic examination of isogenic L. maculans isolates and B. napus introgression lines demonstrated a lack of effect of AvrLm1 on Rlm7-mediated resistance despite an apparent alteration of the Rlm7-dependent defence response using more diverse fungal isolates with differences in AvrLm1 and AvrLm4. As deployment of Rlm7 resistance in crop cultivars increases, other effectors need to be monitored because they may alter the predominance of AvrLm7. © 2023 The Authors. Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.
| Original language | English |
|---|---|
| Number of pages | 8 |
| Journal | Pest Management Science |
| Early online date | 28 Mar 2023 |
| DOIs | |
| Publication status | E-pub ahead of print - 28 Mar 2023 |
Keywords
- Research Article
- Research Articles
- apoplast
- effector
- gene expression
- reactive oxygen species
- R gene‐mediated resistance
- symptoms
- R gene-mediated resistance