ROLE OF PATHOGEN-DERIVED EFFECTOR PROTEINS IN PLANT DISEASE AND RESISTANCE

Plants are exposed to pathogens like fungi, bacteria, viruses and nematodes. The proteins from pathogens have dual functions in host pathogen interaction. Virulent determinants of pathogen cause disease in plants while avirulent determinants elicit defense reactions in host by expressing the appropriate resistance genes (Klaas et al., 2002). Effectors are pathogen molecules that manipulate host cell structure and function, thereby facilitating infection or triggering defense responses.

Phytophthora sojae encodes cytoplasmic effectors with conserved FLAK motifs following signal peptides termed as “crinkling and necrosis-inducing proteins” (CRN).  Out of five P. sojae-specific CRN-like genes three are putative pseudogenes and two functional genes which encode proteins. The PsCRN63 induces cell death while, PsCRN115 suppresses cell death elicited by the P. sojae necrosis inducing protein. The predicted nuclear localization signal is required for PsCRN63 to induce cell death but not for PsCRN115 to suppress cell death (Tingli Liu et al., 2011).

 Pseudomonas syringae pv. tomato DC3000 is a model pathogen for studying the molecular basis of plant immunity and disease susceptibility in tomato and arabidopsis. DC3000 uses a type III secretion system to inject effector proteins into the plant cell. Type III effectors are known to promote bacterial virulence by suppressing plant defenses and enhancing access to nutrients trapped in the plant cell. The AvrPtoB type III effector elicits immunity-associated programmed cell death (PCD) when expressed in tomato plants carrying the Pto resistance protein. However, in the absence of Pto, AvrPtoB functions to suppress PCD and immunity in tomato (Robert et al., 2005).

 Jeffrey et al. (2008) reported that plant innate immunity relies on the recognition of pathogen effector molecules by nucleotide binding-leucine rich repeats (NB-LRRs). The N immune receptor is a member of TIR-NB-LRR family which indirectly recognizes the 50-kDa helicase (p50) domain of Tobacco mosaic virus (TMV) through its TIR domain. The NRIP1 is required for N to provide complete resistance to TMV. N gene activation requires a pre-recognition complex containing the p50 effector and NRIP1.

Root-knot nematodes (RKN) are obligate parasites which establish relationship with host by secreting effectors that suppress host defense. The Mi-CRT, a calreticulin (CRT) secreted by the nematode into the apoplasm of infected tissues plays an important role in infection. The transformed Arabidopsis thaliana plants producing the Mi-CRT were more susceptible to nematode infection than wild-type plants (Jaouannet et al., 2012).                 

The effectors are the valuable tools in understanding the molecular basis of plant pathogen interactions. The increasing number of pathogen factors have shown dual function in virulence and recognition by the host suggesting evolution of a plant recognition system that targets important pathogen virulence factors. This natural strategy provides the blue-print for genetic engineering strategies and to improve crop protection by identifying and targeting critical pathogen factors to evolve more durable resistance.

Selected References:

JAOUANNET, M., MAGLIANO, M., ARGUEL, M. J., GOURGUES, M., EVANGELISTI, E., ABAD, P. AND ROSSO, M. N., 2012, The root-knot nematode calreticulin Mi-CRT is a key effector in plant defense suppression. Pl. physiol., 26(1): 97–105.

JEFFREY, L. C., PADMAVATHI, M., TESSA, M. B., KIRK, C. AND DINESH-KUMAR, S. P., 2008, Chloroplastic protein NRIP1 mediates innate immune receptor recognition of a viral effector. Cell, 132(3): 449–462.

  ROBERT, B., ABRAMOVITCH, GREGORY, B. AND MARTIN ., 2005, AvrPtoB: A bacterial type III effector that both elicits and suppresses programmed cell death associated with plant immunity. Euro. Micro .Soci ., 245 :1–8.

TINGLI LIU, WENWU YE, YANYAN RU, XINYU YANG, BIAO GU, KAI TAO, SHAN LU, SUOMENG DONG, XIAOBO ZHENG, WEIXING SHAN, YUANCHAO WANG. AND DAOLONG DOU., 2011, Two host cytoplasmic effectors are required for pathogenesis of Phytophthora sojae by suppression of host defenses. Pl. Physiol., 155: 490-501.