P-240 - Elucidating the Role and Molecular Mechanism of Heat Shock Factor-Like Transcription Factors in Plant Virus Immunity

The endoplasmic reticulum (ER) is responsible for protein synthesis, folding, and modification. Nevertheless, both biotic and abiotic stresses can affect its function, leading to the accumulation of misfolded or unfolded proteins, thereby triggering ER stress. ER stress has been reported to be induced by viral infection. This may occurs through two mechanisms: promoting the formation of viral replication complexes in the ER and triggering the accumulation of the plant hormone salicylic acid (SA), which plays a key role in virus resistance. To alleviate this stress, cells initiate the unfolded protein response (UPR) for maintaining ER stability. Previous studies have shown that certain UPR genes are involved in viral resistance and SA signaling; however, the regulatory mechanisms remain largely elusive. Our preliminary findings indicate that the UPR-related gene, TBF1 (TL1 binding factor 1), is an HSF-like transcription factor and involved in the expression of SA marker genes. Furthermore, we found that tbf1 mutant plants showed higher accumulation level of both tobacco mosaic virus and cucumber mosaic virus. More importantly, we found that TBF1 is involved in the regulation of RNA interference (RNAi)-related genes. Our study suggested that TBF1 may plays a crucial role in virus resistance by regulating both the SA and RNAi pathways, providing new insights into the role of UPR-related genes in antiviral immunity.