Sp1 and Sp3 regulate basal transcription of the survivin gene

Survivin, a unique member of the inhibitor of apoptosis protein family, is overexpressed in many cancers and considered to play an important role in oncogenesis. In this study, we cloned and identified the proximal 269 bp promoter of survivin gene, which exhibited strong promoter activity in HeLa cells. The TATA-less, GC-rich promoter contains 7 putative binding sites for Sp1, two of which (one at position -148 to -153, the other at position -127 to -140) are essential in regulating basal survivin promoter activity. Not only Sp1 but also Sp3 can activate the survivin promoter, which were proven by EMSA, blocking Sp1 or Sp3 using RNAi or mithramycin treatment of HeLa cells, and overexpression of Sp1 or Sp3. Our results collectively suggest that Sp1 cooperates with Sp3 to regulate survivin promoter activity.     

Palmitate increases Nur77 expression by modulating ZBP89 and Sp1 binding to the Nur77 proximal promoter in pancreatic β-cells

Nur77 is a stress sensor in pancreatic β-cells, which negatively regulates glucose-stimulated insulin secretion. We recently showed that a lipotoxic shock caused by exposure of β-cells to the saturated fatty acid palmitate strongly increases Nur77 expression. Here, using dual luciferase reporter assays and Nur77 promoter deletion constructs, we identified a regulatory cassette between −1534 and −1512 bp upstream from the translational start site mediating Nur77 promoter activation in response to palmitate exposure. Chromatin immunoprecipitation, transient transfection and siRNA-mediated knockdown assays revealed that palmitate induced Nur77 promoter activation involves Sp1 recruitment and ZBP89 release from the gene promoter.     

Biological Control of Take-all Disease of Wheat Caused by Gaeumannomyces graminis var. tritici Under Field Conditions Using a Phialophora sp.

A Phialophora sp. (isolate I-52), originally isolated from soil in a wheat field exhibiting suppression of take-all disease caused by Gaeumannomyces graminis var. tritici , was tested under field conditions for its ability to suppress this disease in winter and spring wheat. I-52 was grown on a variety of autoclaved organic substrates, including oat, millet and canola seed. All of these gave significant disease control when added to the seed furrow with inoculum of the take-all fungus. W hole seed of I-52 substrate was as effective as particles < 0.5 mm in diameter. Placing I-52 in powdered form directly on to wheat seed was ineffective in controlling take-all. Rates as low as 2 g of I-52/3.3 m of row added with the seed provided some control of take-all, and nearly complete control in winter wheat was obtained using 15 g/3.3 m. The winter wheat host cultivar did not influence the degree of control of take-all by I-52.