Hassan Beenish, Bhutto Sadam Hussain, Yin Xiao-Xiao, Yan Xiu-Lian, Liao Rong, Guo Mao-Lin, Tang Ya-Ping, Guo Dai-Ming, Yang Si-Jia, Gulzar Faiza, Li Yan, Zeng Xian-Yin, Zhao Zhi-Xue, Wang Wen-Ming
State Key Laboratory of Crop Gene Exploration and Utilization in Southwest China, Sichuan Agricultural University, Chengdu, China.
Rice Research Institute, Sichuan Agricultural University, Chengdu, China.
Front Plant Sci. 2025 Feb 24;16:1547593. doi: 10.3389/fpls.2025.1547593. eCollection 2025.
Rice blast disease, caused by , poses the most devastating threat to global rice production. The products of most blast resistance () genes specifically recognize corresponding a virulence effectors from the pathogen, thereby mediating robust immune responses that are crucial for disease resistance. However, it is unclear why different genes endow with differential amplitudes of immunity against . . Here, we demonstrated that different blast genes confer differential amplitudes of immunity against . , presumably due to divergent reprogramming of transcriptional responses. We detected that three rice restorer lines exhibited differential amplitudes of immune responses, despite all lines displaying resistance to . . Consistently, different accessions carrying different single genes exhibited remarkable differentially expressed genes (DEGs) count, indicating different transcriptional re-programming that leads to different fitness cost. Comparative analysis revealed varying degrees of overlap among DEGs across different accessions. By integrating RNA-seq and RT-qPCR data, we recommended some marker genes that distinguish the differential amplitude of immunity against . mediated by different blast genes. Thus, our study provides valuable insights into the specific and overlapping roles of gene-mediated immunity. We also propose marker genes that can be used to effectively evaluate the amplitude of immune responses to . , thereby facilitating the assessment of genes with relatively lower amplitude of immunity in order to minimize fitness cost.
稻瘟病由[病原体名称未给出]引起，对全球水稻生产构成最具毁灭性的威胁。大多数抗稻瘟病（[抗病基因名称未给出]）基因的产物特异性识别来自病原体的相应毒性效应子，从而介导对抗病至关重要的强大免疫反应。然而，尚不清楚为什么不同的[抗病基因名称未给出]基因赋予对[病原体名称未给出]的免疫幅度不同。在这里，我们证明不同的稻瘟病[抗病基因名称未给出]基因赋予对[病原体名称未给出]的免疫幅度不同，这可能是由于转录反应的不同重编程所致。我们检测到三个水稻恢复系表现出不同幅度的免疫反应，尽管所有品系都对[病原体名称未给出]具有抗性。同样，携带不同单个[抗病基因名称未给出]基因的不同种质表现出显著不同的差异表达基因（DEG）计数，表明不同的转录重编程导致不同的适合度代价。比较分析揭示了不同种质间DEG的不同程度重叠。通过整合RNA-seq和RT-qPCR数据，我们推荐了一些标记基因，这些基因可区分由不同稻瘟病[抗病基因名称未给出]基因介导的对[病原体名称未给出]免疫的差异幅度。因此，我们的研究为[抗病基因名称未给出]基因介导的免疫的特定和重叠作用提供了有价值的见解。我们还提出了可用于有效评估对[病原体名称未给出]免疫反应幅度的标记基因，从而便于评估免疫幅度相对较低的[抗病基因名称未给出]基因，以尽量减少适合度代价。
