Abstract
The fungus Leptosphaeria maculans (L. maculans) is the causal agent of blackleg disease of canola/oilseed rape (Brassica napus) worldwide. We previously reported cloning of the B. napus blackleg resistance gene, LepR3, which encodes a receptor-like protein. LepR3 triggers localized cell death upon recognition of its cognate Avr protein, AvrLm1. Here, we exploited the Nicotiana benthamiana model plant to investigate the recognition mechanism of AvrLm1 by LepR3. Co-expression of the LepR3/AvrLm1 gene pair in N. benthamiana resulted in development of a hypersensitive response (HR). However, a truncated AvrLm1 lacking its indigenous signal peptide was compromised in its ability to induce LepR3-mediated HR, indicating that AvrLm1 is perceived by LepR3 extracellularly. Structure-function analysis of the AvrLm1 protein revealed that the C-terminal region of AvrLm1 was required for LepR3-mediated HR in N. benthamiana and for resistance to L. maculans in B. napus. LepR3 was shown to be physically interacting with the B. napus receptor like kinase, SOBIR1 (BnSOBIR1). Silencing of NbSOBIR1 or NbSERK3 (BAK1) compromised LepR3-AvrLm1-dependent HR in N. benthamiana, suggesting that LepR3-mediated resistance to L. maculans in B. napus requires SOBIR1 and BAK1/SERK3. Using this model system, we determined that BnSOBIR1 and SERK3/BAK1 are essential partners in the LepR3 signaling complex and were able to define the AvrLm1 effector domain.
Highlights
Plants mainly rely on induced innate immune system to resist pathogen infection
The lack of hypersensitive response (HR) by the full length AvrLm1 is likely due to inefficient secretion of AvrLm1 as directed by its native signal peptide in N. benthamiana plants. These results indicate that AvrLm1 was able to activate LepR3 leading to the development of HR and that the recognition occurred outside the plant cell which is in accordance with LepR3 being a cell surface receptor
Race-specific resistance against L. maculans remains the only practical approach to control blackleg disease of canola (Raman et al, 2013). The genetics of this race-specific resistance have been studied in detail; the molecular mechanism of L. maculans perception by B. napus remained unknown until the cloning of LepR3 and Rlm2, two B. napus R genes against blackleg (Larkan et al, 2013; Larkan et al, 2015)
Summary
Plants mainly rely on induced innate immune system to resist pathogen infection. Membranelocalized pattern-recognition receptors (PRRs) form the first layer of defense by detecting conserved microbe or pathogen-associated molecular patterns (MAMPs or PAMPs) and activating PAMP-triggered immunity (PTI; Jones and Dangl, 2006). One of the PRRs that has been studied extensively is FLAGELLIN SESING 2 (FLS2) that recognizes the bacterial PAMP flagellin 22 (flg22; Cook et al, 2015). FLS2 is a leucine-rich repeat receptor-like kinase (LRR-RLK) and requires another LRR-RLK, the brassinosteroid receptor BRASSINOSTEROID INSENSITIVE 1 -ASSOCIATED KINASE 1 (BAK1)/SERK3, for perception of flg (Ben Khaled et al, 2015). Specialized pathogens have evolved strategies to overcome PTI by secretion of effector proteins
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