Bioscience Evidence 2025, Vol.15, No.6, 270-279 http://bioscipublisher.com/index.php/be 271 different pathogens, especially the regulatory methods in different genotypes and different tissues (such as grains), many of which remain unclear (Nida et al., 2021). Further clarifying the molecular defense mechanism of sorghum can not only help us better understand its genetic basis for disease resistance, but also provide new theories and more specific targets for breeding disease-resistant varieties and conducting more sustainable disease management. 2 Overview of the Immune System of Sorghum 2.1 Basic immunity (PTI) The basic immunity (PTI) of sorghum is its first line of defense against pathogen invasion. This process mainly relies on pattern recognition receptors (PRRs) on the cell membrane. These recipients can recognize the molecular characteristics (PAMPs) of pathogens, such as flagellin or chitin, and then activate subsequent defense signals (Cui et al., 2021) (Figure 1). Once PTI is activated, a series of reactions will occur rapidly in plants, such as increased reactive oxygen species (ROS), stronger cell walls, production of some antibacterial substances, and initiation of the expression of many defense genes (Ding et al., 2022). In sorghum, after the addition of PAMP, the expressions of many PRR and defension-related genes will increase, thereby enhancing resistance to multiple pathogens (Jiang et al., 2023). In addition, the post-translational modification processes of some proteins (such as acetylation) can also affect PTI, altering the activity and stability of defense proteins. Figure 1 Effect of leaf position on the ROS response to MAMP elicitation in sorghum genotypes BTx623 and SC155-14E. (A) Fifteen-day old BTx623 and SC155-14E plants. The leaves from bottom to top were marked as leaf #1 (older leaf), leaf #2 (2nd youngest leaf) and leaf #3 (youngest leaf). (B) ROS response to flg22 or chitin elicitation of all three leaves of fifteen-day old BTx623 and SC155-14E plants. RLU, relative light units; Error bars indicate±SEM; n = 8; * <0.05 (t test) and ** <0.01. (C) Time course of flg22-triggered and chitin-triggered ROS production in leaf # 2 of SC155-14E (Adopted from Cui et al., 2021) 2.2 Effector triggering immunity (ETI) When pathogens secrete effectors and attempt to inhibit PTI, plants initiate a second line of immunity, namely effector triggered immunity (ETI). ETI is mainly mediated by intracellular resistance proteins, many of which are NLR receptors. They can directly or indirectly identify these effectors and then trigger stronger and more targeted defense responses (Nguyen et al., 2021; Khan et al., 2025). ETI is often accompanied by rapid programmed cell death (HR) to prevent the further spread of pathogens and promote systemic resistance formation (Guo and Cheng, 2022; Yu et al., 2024). ETI not only enhances the expression of PTI-related genes, but also makes ROS burst stronger, and the signal transduction response faster and more persistent.
RkJQdWJsaXNoZXIy MjQ4ODYzNA==