Project description:To verify the pathogenicity of Lecanicillium psalliotae invasive pathogens on tsearch leaves, Lecanicillium psalliotae was identified by isolation and purification. sweet orange leaves were infested with it. The results of the experiments showed that 15 days after Lecanicillium psalliotae infested the leaves of sweet orange, yellow spots grew around the pores and irregular yellow spots appeared on both sides of the leaf veins. This was highly similar to the disease in the field, suggesting that Lecanicillium psalliotae is the causal agent of the yellow spots on sweet orange leaves that cause the leaves to wilt and fall off. In previous studies, Verticillium cutaneum was mainly identified as a biological control agent and a suspected pathogen. In this study, the pathogenicity of Verticillium cutaneum was verified for the first time as a causal agent of leaf spot disease of plants.
Project description:FUSCA3 (FUS3) is a B3 domain transcription factor that is a member of the LEAFY COTYLEDON (LEC) group of genes. The LEC genes encode proteins that also include LEC2, a B3 domain factor related to FUS3, and LEC1, a CCAAT box binding factor. LEC1, LEC2 and FUS3 are essential for plant embryo development. We report ChIP-chip experiments using the Affymetrix tiling array to globally map binding sites for FUS3. Fangfang Wang and Sharyn E. Perry (2013) Plant Physiology preview
Project description:Ikaros DNA binding proteins are important regulators of haematopoiesis and genetic deletion of Ikaros results in severe developmental disturbances, including delayed thymocyte differentiation and an early and complete block in B cell development. Although Ikaros ChIP-seq data are available for mouse thymocytes and human haematopoietic progenitors, it has not been achieved in B cell progenitors. The goal of this study was to identify Ikaros binding sites in pre-B cells to define Ikaros target genes which could explain the essential role of Ikaros proteins in B cell differentiation. We carried out chromatin immunoprecipitation and high throughput sequencing (ChIP-seq) with antibodies to the C-terminus of endogenous Ikaros in B3 cells and with anti-haemagglutinin (HA) in B3 cells transduced with epitope-tagged HA-Ikaros.