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.