Sustainable cherry defense: MAMPs receptors and carotenoids in Lapins cultivar

19 Nov 2025
1775

Sweet cherry is a species highly vulnerable to pathogens such as Pseudomonas syringae pv. syringae, the causal agent of bacterial canker, and Botrytis cinerea, responsible for fruit gray mold.

The economic losses associated with these diseases have driven research toward new defense strategies that combine efficacy and sustainability.

A recent study investigated the role of plant innate immunity, particularly that activated by microorganism-associated molecular patterns (MAMPs), and its connection with carotenoid metabolism, focusing on the cultivar “Lapins”.

Identification of immune receptors

The study identified and characterized two pattern-recognition receptors (PRRs) in sweet cherry, named PaEIX2 and PaFLS2, homologous to tomato genes SlEIX2 and SlFLS2, respectively.

These receptors recognize two well-known MAMPs: the ethylene-inducing xylanase (xyn11/eix), of fungal origin, and the peptide flg22 derived from bacterial flagellin.

Both receptors, localized in the plasma membrane, were confirmed to be functional and capable of activating pattern-triggered immunity (PTI), a key mechanism in the plant defensive response.

In assays conducted in tobacco, their expression induced the production of reactive oxygen species (ROS) and, in the case of PaEIX2, also programmed cell death, a typical defense mechanism against necrotrophic pathogens.

Differential responses to elicitors

In sweet cherry, the two elicitors triggered differential responses: flg22 markedly reduced susceptibility to P. syringae, while xyn11/eix showed greater effectiveness against B. cinerea.

At the physiological level, treatment with flg22 stimulated the biosynthesis of abscisic acid (ABA), whereas xyn11/eix increased ethylene production, confirming the activation of distinct hormone pathways specific to each type of pathogen.

Carotenoids and PTI activation

The study also examined the role of carotenoids, plant pigments with antioxidant functions and precursors of bioactive metabolites known as apocarotenoids, during PTI activation.

Although the total carotenoid content did not increase following elicitation, the genes involved in carotenoid metabolism displayed differential regulation, suggesting a qualitative rather than quantitative remodeling and the possible production of apocarotenoids with defensive signaling functions, such as β-cyclocitral, β-ionone, or ABA itself.

Moreover, the exogenous application of carotenoids reduced cherry susceptibility to P. syringae even in the absence of elicitors, indicating a potential immune-priming effect.

However, this treatment did not enhance the defense induced by flg22 or xyn11/eix and proved ineffective against B. cinerea, suggesting a complex interaction between carotenoid metabolism and the defense pathways activated by PTI.

Conclusions and future perspectives

This result highlights that, although carotenoids and their derivatives may play a regulatory role, their influence depends on the type of pathogen and on the plant’s physiological state.

In conclusion, PaEIX2 and PaFLS2 are active and functional receptors in MAMP perception, and their activation elicits distinct yet complementary defensive responses in cherry.

The integration between molecular immunity and carotenoid metabolism opens new perspectives for sweet cherry protection, with potential applications in varietal selection and in the development of biostimulants or resistance-inducing treatments.

Further research on the regulatory mechanisms of apocarotenoids and their interaction with hormonal pathways could lead to advanced and sustainable phytosanitary strategies for fruit crops, reducing the use of conventional pesticides and improving crop resilience to emerging pathogens.

Source: Álvarez González, A. S. (2025). Rol funcional del metabolismo de Carotenoides durante la inmunidad gatillada por patrones moleculares en Prunus avium cv. Lapins. https://repositorio.uchile.cl/handle/2250/205663 

Image source: Pswwarndienst

Andrea Giovannini
University of Bologna (IT) 


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