MOLECULAR-INTERACTIONS OF BIPOLARIS-MAYDIS T-TOXIN AND MAIZE

The toxins (T-toxins) produced by the fungal pathogens Bipolaris maydi s race T (BmT) and Phyllosticta maydis (Pm) target the mitochondrial r eceptor, URF13, in maize (Zea mays L.) plants containing the Texas mal e-sterile cytoplasm (cms-T). URF13, a 13-kDa protein, is the product o f the maize mitochondrial gene T-urf13, which is found only in the mit ochondrial genome of cms-T maize and is thought to be responsible for cytoplasmically inherited male sterility and disease susceptibility. P m-toxin binds specifically to URF13 in a cooperative manner, and Pm- a nd BmT-toxins compete for the same, or overlapping, binding sites. The binding of T-toxin to URF13 causes rapid permeabilization of the inne r mitochondrial membrane, which results in leakage of NAD(+) and other ions from the matrix. A pore consisting of at least six transmembrane alpha-helices is required for NAD(+) leakage. Cross-linking experimen ts showed that URF13 oligomers are present in the mitochondrial membra ne. A model of the secondary structure of URF13 proposes that each mon omer contains three transmembrane alpha-helices. Studies combining sit e-directed mutagenesis and chemical cross-linking of URF13 expressed b y Escherichia coli cells indicate that the oligomers are composed of a central core of helices II that line the center of the URF13 pores.