Plant resist disease through a many preformed and induced barrier to infection and therefore the pathogen uses virulence factors to overcome plant defenses and infect (Sacristan and Garcia-Arenal 2008). Virulence factors are molecules that enable plant pathogens to infect and colonize host tissue. These molecules co-evolve with host genes to ensure functionality and evade recognition by host immune system (Spallek et al., 2018). With the ever-evolving toolset of virulence factors, pathogen challenge plants in an environment. The toolset comprises of small, secreted effector proteins, RNAs and toxins. Several of the virulence factor show high degree of species and strain specificity (Spallek et al., 2018). Plant fungal and bacterial pathogens produce many phytotoxins, which are crucial determinants of pathogenicity (the capacity to cause plant disease) (Strange 2007), or virulence (the degree of pathogenicity) (Walton 2006; Speth et al., 2007).
Pathogens can infect wide host plant range and are rarely restricted to a single host and most hosts are exposed to more than one pathogen species Majority of pathogens can infect many closely related species and some wide taxonomic range of hosts (Woolhouse et al., 2001). A pathogen can acquire a new host plant depends on the genetic compatibility between the two, either through preadaptation of the pathogen or by evolutionary change (Parker and Gilbert 2004). The outcome of pathogen infection varies with plant resistance and tolerance to infection (Barrett et al., 2009). Virulence is the detrimental effect of pathogens on host plant fitness. It reduces life span of the plant which results in decreased fecundity (seed production) and hence, a decrease in its fitness. Pathogenicity is the ability of the pathogen to cause disease on a specific host- it is a qualitative term. Virulence is a quantitative measurement of pathogenicity indicating the degree of damage caused on the host and is assumed to have a negative effect on the host fitness (Parker and Gilbert 2004). Virulence is not necessarily correlated with factors that determine pathogens fitness such as efficiency with which a pathogen uses the host plant as substrate or its ability to colonize a new plant (Parker and Gilbert 2004). Plant disease development requires three components such as i) a susceptible host, ii) a virulent pathogen and c) favorable environmental conditions. Even if a virulent pathogen is present in an environment with genetically susceptible host, and if the environmental conditions (moisture, temperature or soil conditions) are not conducive it may prevent disease development (Velasquez et al., 2018).
The absence or presence of certain virulence factor has influence on the rate of infection dissemination. Virulence factors are divided into four groups: adhesion factors, invasion factors, toxin factors and immune evasion factors (Abdulateef et al., 2023). Few microorganisms may evade host immune recognition. Virulence parameters expression can be influenced by various genetic and environmental variables including quorum sensing (Alspaugh 2015; Abdulateef et al., 2023). Quorum sensing is a cell-cell communication process that enables microbial cell to obtain information about cell density and species composition in the vicinity and adjust their gene expression profile accordingly (Papenfort and Bassler 2016; Padder et al., 2018). During the initial encounter, the pathogen senses the host environment and respond to the adaptive cellular changes. Pathogen adapts to the prevailing condition by modulating its gene expression. The product of such gene facilitates survival and proliferation of the bacterial pathogen or cause damage to the host are considered as virulence or pathogenicity determinants (Thomas and Wigneshweraraj 2015).
Plant disease resistance and susceptibility are governed by the combined genotype of the host and the pathogen, which depends on the complex exchange of the signals and responses occurring under given environmental condition (Yang et al.,1997). Plant pathogen causing disease on a particular host is regulated by gene-for-gene interaction i.e. the plant has resistance (R) gene and the pathogen has corresponding specific avirulence (Avr) gene, the plant gene-for-gene defense pathway is activated (Dangl 1995; Yu et al., 1998). The Avr gene encode for products (effector proteins) secreted into the plant cell to promote pathogen virulence and to overcome host plant defense responses. The Avr gene products on being recognized by the corresponding R gene lead to an incompatible interaction (resistant) (Parker and Gilbert 2004). Pathogen lacking those Avr genes are termed virulent on that host plant. The combination of Avr genes in a pathogen strain determines the race of the pathogen (Flor 1956). The avirulence factor elicit avirulence responses in the host plant such as hypersensitive response at the infection site. The non-virulent pathogen in an incompatible reaction does not colonize the plant and the plant is not diseased and does not develop any symptoms. A virulent pathogen in a compatible (susceptible) interaction is not recognized by the host plant, even if pathogen harbors an Avr gene (Surico 2013). The pathogen then colonizes the plant and cause disease and develop symptoms.
To optimize defense against pathogens with distinct lifestyles, plant depend on hormonal networks to fine-tune specific responses and regulate growth-defense tradeoff. Several pathogens also produce plant hormones (Chanclud and Morel 2016; Ma and Ma 2016). The hormones abscisic acid, gibberellic acid and ethylene produced by the fungi participate in pathogenicity (Chanclud and Morel 2016). Auxins and cytokinins (CK) are regulators required for virulence (Chanclud and Morel 2016). Past studies reveal that plant-pathogenic fungus Claviceps purpurea produces CK, highlights the biosynthesis and function of these plant hormones (Hinsch et al., 2016). CK is a virulence factor because the CK produced by different plant pathogens hijack host CK signaling cues to increase host susceptibility and cause plant diseases and parasitism (Spallek et al., 2018). Advances has been made in characterizing the host plant target of viral and bacterial virulence factor, providing an insight into plant basic cellular processes such as gene silencing, vesicle trafficking, hormone signaling and innate immunity (Speth et al., 2007). To control plant disease, one must understand how pathogen shape plant development to increase virulence and cause disease.
References:
Abdulateef, S. A., Aal Owaif, H. A. and Hussein, M. H. 2023 Importance of Virulence Factors in Bacterial Pathogenicity: A Review. IJMSCRS 3(4): 765 – 769
doi.org/10.47191/ijmscrs/v3-i4-35
Alspaugh, J. A. 2015 Virulence Mechanisms and Cryptococcus neoformans Pathogenesis. Fungal Genetics and Biology 78: 55 – 58
doi.org/10.1016/j.fgb.2014.09.004
Barrett, L. G., Kniskern, J. M., Bodenhausen, N., Zhang, W. and Bergelson, J. 2009 Continua of Specificity and Virulence in Plant Host-Pathogen Interactions: Causes and Consequences. New Phytologist 183(3): 513 – 529
doi.org/10.1111/j.1469-8137.2009.02927
Chanclud, E. and Morel, J-B. 2016 Plant Hormones: A Fungal Point of View. Mol. Plant Pathol. 17(8): 1289 – 1297
doi.org/10.1111/mpp.12393
Dangl, J. L. 1995 Piece de Resistance: Novel Classes of Plant Disease Resistance Genes. Cell 80(3): 363 – 366
doi: 10.1016/0092-8674(95)90485-9
Flor, H. H. 1956 The Complementary Genic Systems in Flax and Flax Rust. Adv. Gen. 8: 29 – 54
doi.org/10.1016/S0065-2660(08)60498-8
Hinsch, J., Galuszka, P. and Tudzynski, P. 2016 Functional Characterization of the First Filamentous Fungal tRNA-Isopentenyltransferase and Its Role in the Virulence of Claviceps purpurea. New Phytologist 211(3): 980 – 992
doi.org/10.1111/nph.13960
Ma, K-W. and Ma, W. 2016 Phytohormone Pathways as Targets of Pathogens to Facilitate Infection. Plant Mol. Biol. 91: 713 – 725
Padder, S. A., Prasad, R. and Shah, A. H. 2018 Quorum Sensing: A Less Known Mode of Communication Among Fungi. Microbiol. Res. 210: 51 – 58
Doi.org/10.1016/j.micres.2018.03.007
Papenfort, K. and Bassler, B. L. 2016 Quorum Sensing Signal-Response Systems in Gram-negative Bacteria. Nat. Rev. Microbiol. 14: 576 -588
Parker, I. M. and Gilbert, G. S. 2004 The Evolutionary Ecology of Novel Plant-Pathogen Interactions. Annu. Rev. Ecol. Evol. Syst. 11(35): 675 – 700
doi: 10.1146/annurev.ecolsys.34.011802.132339
Sacristan, S. and Garcia-Arenal, F. 2008 The Evolution of Virulence and Pathogenicity in Plant Pathogen Populations. Mol. Plant Pathol. 9(3): 369 – 384
doi: 10.1111/j.1364-3703.2007.00460.x .
Spallek, T., Gan, P., Kadota, Y. and Shirasu, K. 2018 Same Tune, Different Song-Cytokinins as Virulence Factors in Plant-Pathogen Interactions? Curr. Opin. Plant Biol. 44: 82 – 87
doi.org/10.1016/j.pbi.2018.03.002
Speth, E. B., Lee, Y. N. and He, S. Y. 2007 Pathogen Virulence Factors as Molecular Probes of Basic Plant Cellular Functions. Curr. Opin. Plant Biol. 10(6): 580 – 586
doi: 10.1016/j.pbi.2007.08.003
Strange, R. N. 2007 Phytotoxins Produced by Microbial Plant Pathogens. Nat. Prod. Rep. 24(1): 127 – 144
doi: 10.1039/b513232k
Surico, G. 2013 The Concepts of Plant Pathogenicity, Virulence/Avirulence and Effector Proteins by a Techer of Plant Pathology. Phytopathologia Mediterranea 52(3): 399 – 417
doi.org/10.14601/Phytopathol_Mediterr-12077
Thomas, M. S. and Wigneshweraraj, S. 2015 Regulation of Virulence Gene Expression. Virulence 5(8): 832 – 834
doi: 10.1080/21505594.2014.995573
Velasquez, A. C., Castroverde, C. D. M. and He, S. Y. 2018 Plant and Pathogen Warfare under Changing Climate Conditions. Curr. Biol. 28(10): R619 – R634
doi: 10.1016/j.cub.2018.03.054
Walton, J. D. 2006 HC-Toxin. Phytochem. 67(14): 1406 – 1413
doi.org/10.1016/j.phytochem.2006.05.033
Woolhouse, M. E., Taylor, L. H. and Haydon, D. T. 2001 Population Biology of Multihost Pathogens. Science 292(5519): 1109 -1112
doi: 10.1126/science.1059026
Yang, Y., Shah, J. and Klessig, D. F. 1997 Signal Perception and Transduction in Plant Defense Responses. Genes and Dev. 11(13): 1621 – 1639
doi: 10.1101/gad.11.13.1621
Yu, I-C., Parker, J. and Bent, A. F. 1998 Gene-for-Gene Disease Resistance without the Hypersensitive Response in Arabidopsis dnd1 Mutant. 95(13): 7819 – 7824
doi.org/10.1073/pnas.95.13.7819
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