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Summary: Regulation of host gene expression to promote disease is a common strategy for plant pathogens. However, it remains unclear whether or not fungal pathogens manipulate host gene expression directly through secreted effectors with transcriptional activity.Here, we identified a fungal effector PstGTA1 from Puccinia striiformis f. sp. tritici (Pst), which has partial homology to the subunit of global transcriptional activator SNF2 from oyster. The transcriptional activating activity of PstGTA1 was validated in yeast, and the potential role of PstGTA1 in pathogenicity was assessed using gene silenced and overexpression transgenic wheat plants. Candidate targets regulated by PstGTA1 were screened by transcriptomic analysis, and the specific promoter region binding to PstGTA1 was further determined.PstGTA1 can be delivered to the wheat cell nucleus and contributes to the full virulence of Pst by targeting the promoter of TaSIG, a gene negatively regulating wheat immunity, and possibly activates its transcription by affecting the histone H3K4 acetylation level.Our study provides the first direct evidence for a fungal effector with transactivation activity modulating the transcription of a host specific susceptibility gene through promoter binding and histone acetylation. [ABSTRACT FROM AUTHOR]

Objective: Interferon-α (IFNα) therapy has been an integral part of the current treatment for hepatitis B virus (HBV) infection. However, the exact effect of IFNα antiviral therapy on liver function and iron metabolism in patients with chronic hepatitis B (CHB) remains unclear. Here, we investigated the characteristics of changes in liver function and iron metabolism indexes in patients with chronic hepatitis B before and after IFNα treatment. Additionally, we determined their predictive value for the therapeutic response of IFNα treatment., Methods: In this study, 34 patients with CHB before and after IFNα treatment were enrolled. Serum levels of virological indicators, liver function, and iron metabolism markers were detected and analyzed in each patient. ROC curve analysis was performed to compare the predictive value of serum liver function and iron metabolism markers for the therapeutic response of IFN α treatment., Results: A significant decrease in serum HBV DNA ( P <0.001) and HBsAg ( P <0.001) was observed before and after IFNα treatment. Compared to the patients before IFNα treatment, patients after IFNα treatment showed a significant increase in serum albumin (ALB) ( P <0.05) and a significant decrease in serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) ( P =0.003 and P =0.034). These findings suggested that the synthetic function of the liver was improved, and liver inflammation was alleviated. Serum HEPC and serum ferritin (SF) levels in patients after IFNα treatment were significantly higher ( P <0.001, P <0.001); however, serum iron (SI) levels were significantly lower ( P =0.005) than those in patients before IFNα treatment. These findings indicate that IFNα treatment regulated iron metabolism homeostasis in CHB patients. Combined liver function and iron metabolism markers, including ALB, SI, SF, and HEPC, had the highest predictive value for the therapeutic response of IFNα treatment for CHB., Conclusion: IFNα treatment improved liver function and iron metabolism homeostasis in patients with CHB. Regular monitoring of serum ALB, SI, SF, and HEPC can help predict the therapeutic response of IFNα treatment for CHB., (© 2024 by the Association of Clinical Scientists, Inc.)