On July 9, 2025, the team of Ning Zhang and Feng Chen from Henan Agricultural University and Xing Wang Deng from Peking University published an article in PNAS titled "TaHSP18.6 and TaSRT1 interact to confer resistance to Fusarium crown rot by regulating the auxin content in common wheat". The study revealed the molecular mechanism by which the TaHSP18.6-TaSRT1 gene module resists disease by regulating auxin, providing a new target for disease resistance breeding.
Fusarium Crown Rot is a plant disease caused by Fusarium pseudograminearum, which mainly affects cereal crops such as wheat, barley and corn. This disease usually causes discoloration and rot of the lower stems and roots of crops, eventually leading to stunted growth or death of plants, which seriously affects crop yields. FCR can cause wheat yield reduction of up to 50%. What is more serious is that the pathogen secretes vomitoxin and other substances that endanger human and animal health, 90% of the world's major wheat varieties are highly susceptible to the disease, the number of reported disease resistance genes is scarce and the effect is limited.
This study identified an 18.6 kDa heat shock protein gene TaHSP18.6 by integrating transcriptome analysis and genome-wide association study (GWAS). EMS mutagenesis and genetic transformation techniques confirmed that TaHSP18.6 positively regulated wheat FCR resistance. Through further screening, the authors found that lysine deacetylase TaSRT1 interacted with TaHSP18.6 and inhibited TaHSP18.6 protein accumulation through deacetylation. In addition, haplotype analysis showed that the K171M mutation of TaHSP18.6 formed the susceptible haplotype TaHSP18.6M171, and mass spectrometry results confirmed that K171 was a key acetylation site.
Then, the authors conducted overexpression and mutant experiments, and the experimental results showed that TaSRT1 negatively regulated wheat FCR resistance. At the same time, the study found that TaHSP18.6 interacted with the auxin response protein TaIAA1 (negatively regulating resistance). Overexpression of TaHSP18.6 and mutation of TaSRT1 significantly increased auxin content, and exogenous application of auxin can greatly enhance wheat FCR resistance.
This study proposed that the TaSRT1–TaHSP18.6 module may regulate wheat FCR resistance by mediating TaIAA1 to change endogenous auxin content.
The research team screened the key gene TaHSP18.6 (a 18.6 kDa heat shock protein) through transcriptome and GWAS, and analyzed its interaction network with the deacetylase TaSRT1.
Multi-omics screening: After inoculation with pathogens, TaHSP18.6 was locked in among 53 differentially expressed genes. Knocking out this gene caused the disease index (DI) to soar by 60%, and overexpressing this gene led to significantly enhanced disease resistance (DI decreased by 45%), while increasing thousand-grain weight (yield increase potential).
Figure 1. TaHSP18.6 and TaSRT1 were verified to regulate wheat Fusarium crown rot resistance. (Zhang, et al., 2025)
TaSRT1 acts as a "deacetylation scissors": Directly binds to and removes the acetylation modification (Kac) of TaHSP18.6, causing TaHSP18.6 to be degraded by the 26S proteasome.
Key site K171: Acetylation site mutation (K171 to M171) causes disease resistance to be lost, and mass spectrometry confirms that K171 is the core action site of TaSRT1.
TaHSP18.6 binds to the auxin inhibitory protein TaIAA1. Releases the transcription factor TaARF6 to activate auxin response genes (SAUR32/71). Spraying auxin (IAA) increases disease resistance of susceptible wheat by 70%. Gene editing TaIAA1 leads to increased auxin accumulation, ultimately leading to enhanced disease resistance.