In many crop production systems, plant diseases brought on by pathogenic microbes continue to be a significant barrier. However, most plants are inaccessible to pathogens due to constitutive and inducible defense systems, making disease an exceptional rather than typical result of plant−microbe interactions. Thus, many plant pathologists were particularly interested in defense mechanisms and associated pathogen resistance, and during the past few decades, molecular mechanisms methods underlying resistance have been clarified. Physiological and molecular factors responsible for effective infection and subsequent disease have recently gained significant scientific attention. The search is now on for the plant compatibility functions that these pathogen effectors are manipulating as well as the effectors that are subverting the host cell. It should be able to design novel plant protection measures based on interfering with compatibility to avoid disease once the molecular pathways driving successful infection are understood. This chapter discusses plant susceptibility and emphasizes on several host mechanisms that have been demonstrated to be generated or mishandled to promote infection. Pattern-triggered immunity is the initial layer of inducible defenses that is triggered by extracellular recognition of molecular patterns (MAMPs and DAMPs) that are linked with pathogen and host (PTI). Since apoplastic colonization of plant-infecting microorganisms is common, all pattern recognition receptors (PRRs) discovered in plants. Recent researchers have found that PRRs significantly differ from one another in terms of their regulation processes and functions, in addition to the shared basic principles underlying PRR signaling. When multiple PRRs are active at once and under attack from microbes during a real infection, this helps to provide the entire PTI system strength and adaptability. We discuss the biological implications and molecular underpinnings of PRR-mediated disease resistance and pathogen recognition, as well as an emerging function for PRRs in homeostatic interaction with commensal or beneficial microbes.

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Molecular Mechanism of Host−Pathogen Interactions

  • Sushma Sharma,
  • Sapna Thakur,
  • Priyanka Thakur,
  • Mahima Kumari,
  • Imran Sheikh

摘要

In many crop production systems, plant diseases brought on by pathogenic microbes continue to be a significant barrier. However, most plants are inaccessible to pathogens due to constitutive and inducible defense systems, making disease an exceptional rather than typical result of plant−microbe interactions. Thus, many plant pathologists were particularly interested in defense mechanisms and associated pathogen resistance, and during the past few decades, molecular mechanisms methods underlying resistance have been clarified. Physiological and molecular factors responsible for effective infection and subsequent disease have recently gained significant scientific attention. The search is now on for the plant compatibility functions that these pathogen effectors are manipulating as well as the effectors that are subverting the host cell. It should be able to design novel plant protection measures based on interfering with compatibility to avoid disease once the molecular pathways driving successful infection are understood. This chapter discusses plant susceptibility and emphasizes on several host mechanisms that have been demonstrated to be generated or mishandled to promote infection. Pattern-triggered immunity is the initial layer of inducible defenses that is triggered by extracellular recognition of molecular patterns (MAMPs and DAMPs) that are linked with pathogen and host (PTI). Since apoplastic colonization of plant-infecting microorganisms is common, all pattern recognition receptors (PRRs) discovered in plants. Recent researchers have found that PRRs significantly differ from one another in terms of their regulation processes and functions, in addition to the shared basic principles underlying PRR signaling. When multiple PRRs are active at once and under attack from microbes during a real infection, this helps to provide the entire PTI system strength and adaptability. We discuss the biological implications and molecular underpinnings of PRR-mediated disease resistance and pathogen recognition, as well as an emerging function for PRRs in homeostatic interaction with commensal or beneficial microbes.