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Immune-related hybrid incompatibility (HI) is one form of post-zygotic reproductive isolation, frequently caused by allelic mismatches of genes involved in plant immunity.

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Abstract

Immune-related hybrid incompatibility (HI) is one form of post-zygotic reproductive isolation, frequently caused by allelic mismatches of genes involved in plant immunity.

Immune-related HI between the North European Landsberg erecta (Ler) and Central Asian Kashmir-2 (Kas-2) Arabidopsis thaliana (A.t.) accessions likely arose as a by-product of adaptation to the biotic environment. It is due to the recessive genetic interaction between a highly variable RECOGNITION OF PERONOSPORA PARASITICA1 (RPP1)-like resistance gene cluster in Ler and Kas-2 alleles of the receptor-like kinase-encoding gene STRUBBELIG RECEPTOR FAMILY 3 (SRF3). Similar to A.t. autoimmune-mutants, this epistasis exposes a temperature-dependent trade-off between immunity and growth. Some RPP1 receptors are known to be involved in pathogen effector recognition, culminating in effector-triggered immunity. However, the precise sub-cellular localization and molecular function of SRF3 in A.t. was still undefined, when this work was initiated. Previous work showed that compatible SRF3-forms (SRF3

Ler

) in Kas-2 backgrounds dampen activation of defensive MPK4 and MPK6 upon perception of the bacterial PAMP-epitope flg22 and enhance susceptibility to Pseudomonas syringae.

The work presented integrates SRF3 in the context of PAMP-triggered

immunity (PTI). SRF3-GFP localizes to the plasma membrane and

plasmodesmata (PD). SRF3

Ler

-GFP-associated proteins identified in a proteomics

approach are enriched for plasmodesmal and plasma membrane proteins

involved in PTI and callose deposition. Contrary to MAPK activation, presence of

SRF3

Ler

in a Kas-2 genetic background leads to enhanced ROS burst and

restriction of PD-flux upon flg22 treatment, but renders Kas-2 almost insensitive to

seedling growth inhibition in the presence of flg22. The results presented, suggest

that SRF3

Ler

differentially affects independent PTI signalling branches

downstream of the PRR complex and provide an example how studying immune-

related HI can be used to identify molecular components involved in plant defence.

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