Infection Strategies and Pathogenicity of Biotrophic Plant Fungal Pathogens

Abstract

Biotrophic plant pathogenic fungi are widely distributed and are among the most damaging pathogenic organisms of agriculturally important crops responsible for significant losses in quality and yield. However, the pathogenesis of obligate parasitic pathogenic microorganisms is still under investigation because they cannot reproduce and complete their life cycle on an artificial medium. The successful lifestyle of biotrophic fungal pathogens depends on their ability to secrete effector proteins to manipulate or evade plant defense response. By integrating genomics, transcriptomics, and effectoromics, insights into how the adaptation of biotrophic plant fungal pathogens adapt to their host populations can be gained. Efficient tools to decipher the precise molecular mechanisms of rust-plant interactions, and standardized routines in genomics and functional pipelines have been established and will pave the way for comparative studies. Deciphering fungal pathogenesis not only allows us to better understand how fungal pathogens infect host plants but also provides valuable information for plant diseases control, including new strategies to prevent, delay, or inhibit fungal development. Our review provides a comprehensive overview of the efforts that have been made to decipher the effector proteins of biotrophic fungal pathogens and demonstrates how rapidly research in the field of obligate biotrophy has progressed.

Keywords: biotrophs; effectors; pathogen-host interaction; pathogenicity; plant fungal pathogens.

FIGURE 1

Illustration of the general infection process of a dikaryotic stage rust fungus. A urediospore (U) attached to an adhesion pad (A) germinate forming germ tubes (GT) which sense the topography of host cuticle and develop appressoria (AP) above stomata (Guard cells—G). Penetration occurs through stomata by the penetration hyphae (PE) into the substomatal spaces where the fungus differentiates into substomatal vesicles (SV) and elongates into an intercellular hypha (IH) which comes into contact with the host mesophyll cells (M) and develops haustorial mother cells (HMC). Following this, haustorial formation is initiated, neckbands (NB) are formed around the site of penetration of the mesophyll cell and an interfacial matrix (IFM) develop between the haustoria cell wall and the cell plasma membrane.