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Valsa pyri is a fatal pathogenic fungus that causes pear and apple canker disease. To date, its cellular development and pathogenicity have been poorly understood. In this study, a V . pyri Ca 2+ /calcineurin-dependent transcription factor CRZ1 (VpCRZ1) is identified and functionally characterized. The △VpCRZ1 mutant exhibits impaired pathogenicity and is no longer able to form fruiting body. Interestingly, this mutant also exhibits enhanced pigment deposition and increased resistance to cell wall perturbing agents including SDS, Congo red and calcofluor white (CFW). The expression levels of Congo red resistance genes ( VpRCR1 and VpRCR2 ) and chitin synthetase genes ( VpCHS2 and VpCHS6 ) are upregulated in the △VpCRZ1 mutant compared to the wild type. Furthermore, We show that a VpCRZ1: eGFP fusion protein localizes to the nucleus in a Ca 2+ -dependent manner similar to its homologs in other fungi, and that the VpFKS1 , VpPMC1 , VpPMC2 , VpPMR1 , and VpPMA1 genes are regulated by VpCRZ1 in response to Ca 2+ levels. Together, these results suggest that VpCRZ1 is a Ca 2+ -dependent transcription factor and required for regulating mycelial morphology, fruiting body formation, and virulence of this important pear and apple pathogen. [ABSTRACT FROM AUTHOR]

Abstract Adipogenesis is one of the key processes during obesity development. Better understanding of this process could advance our knowledge on obesity and its treatment. Transcription factors (TFs) are master regulators during adipogenesis, however, a system-wide analysis of TFs dynamic proteome during adipogenesis is lacking. Here, we profiled 472 TFs and systematically elucidated their roles during the first 7 days of adipogenesis of human adipose-derived stem cells (hADSCs) on proteome scale. We identified two main and four sub-phases during adipogenesis. The commitment phase (0 h–8 h) mainly mediated stem cell proliferation, differentiation and chromatin remodeling, in which proteins of SWI/SNF family are the key centroid nodes. The determination phase (1D-7D) predominately regulated fat cell differentiation and response to lipid and oxygen, which could be associated with terminal differentiation of adipocyte and responsible for maturation. PPARγ, CREB1 and MYC are the centroid nodes of this phase. Remarkably, we identified and verified three TFs (BATF3, MAFF and MXD4) as novel regulators of adipogenesis, whose over-expression could inhibit adipogenesis of hADSCs in vitro. Overall, our study provided a valuable TFs resource to understand the complex process of adipogenesis. Highlights • Systematically depicted dynamic profiles of TFs during adipogenesis of hADSCs at proteome level. • Divided adipogenesis of hADSCs into two main and four sub-stages via dynamic proteome patterns of TFs. • Revealed featured biological responses during different stages of adipogenesis and figured out critical regulatory TFs. • Proposed three novel regulatory TFs (MAFF, BATF3 and MXD4), whose over-expression could inhibit adipogenesis of hADSCs. [ABSTRACT FROM AUTHOR]

Vibrio anguillarum infection can activate NF-κB/TNFα pathway in the immune organs of fish. Fish muscle is also an important immune organ, but the research on its immune function is few. Our aim was to study regulating mechanism of NF-κB and TNFα gene expressions in the muscle of Japanese flounder (Paralichthys olivaceus) which was under Vibrio anguillarum infection (0, 24, 48, 72 and 96 h). The results showed that the expressions of NF-κB and TNFα increased significantly at 48 h, and there was a significant positive correlation between them. In situ hybridization confirmed the co-existence of NF-κB and TNFα genes in Japanese flounder muscle. Interestingly, the expression of the TNFα gene was regulated by the DNA methylation and its methylation level was negatively correlated with the expression. The lowest methylation level of TNFα occurred at 48 h under Vibrio anguillarum infection (P < 0.05). And more, when the fragment (−2122 ∼ −730) was deleted on TNFα gene promoter, double luciferase activity was the highest, indicating that fragment (−730–0) was the transcription factor binding region. The site (−78 ~ −69) on the fragment (−730–0) binding NF-κB was mutated, and double luciferase activity decreased significantly. The results confirmed that the site (−78 ~ −69) was indeed an important binding site for NF-κB. In addition, the activity of TNFα in the serum of Japanese flounder changed with the prolongation of vibrio anguillarum infection, and the concentration of other immune factors such as ALP, ALT, AST and LDH also changed in the muscle under vibrio anguillarum infection. They all showed a trend of first increasing and then decreasing. Above studies implied that Japanese flounder responded to Vibrio anguillarum infection at the immune level with the change of its methylation status and the activation of transcription factor. By studying the mechanism of immune pathways, understanding the response to immune stress is great significant to the research of fish breeding for disease resistance. • Immune stress of NF-κB/TNFα pathway immune gene caused by Vibrio anguillarum infection. • The change of epigenetic DNA methylation modification caused by Vibrio anguillarum infection. • The binding site of transcription factor NF-κB on TNFα promoter region was identified. • DNA methylation regulation and transcription factor worked together on immune regulation. [ABSTRACT FROM AUTHOR]