Mutations in the maize mitochondrial T-urf13 gene eliminate sensitivity to a fungal pathotoxin.
AUTOR(ES)
Braun, C J
RESUMO
URF13, the product of the mitochondrial T-urf13 gene, confers on Texas cytoplasmic male-steril maize (Zea mays L.) a unique susceptibility to a fungal pathogen (Bipolaris maydis race T) and sensitivity to its pathotoxin. Expression of URF13 in Escherichia coli imparts pathotoxin sensitivity to the bacterium. We show by ion uptake studies in E. coli that a pathotoxin-URF13 interaction causes membrane permeability. Similarly, mitochondrial dysfunction caused by membrane permeabilization probably accounts for increased colonization of maize carrying the Texas cytoplasm by toxin-producing pathogens. Site-directed mutagenesis studies show that approximately one-quarter of the amino acids at the carboxyl end of URF13 can be eliminated without affecting toxin sensitivity. We have identified two dicyclohexylcarbodiimide (DCCD) binding sites in the URF13 protein and show that one of the sites is involved in conferring DCCD protection against the pathotoxin. Substitutional mutations at this DCCD binding site also eliminate toxin sensitivity.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=287284Documentos Relacionados
- Targeting the maize T-urf13 product into tobacco mitochondria confers methomyl sensitivity to mitochondrial respiration.
- Expression in yeast of the T-urf13 protein from Texas male-sterile maize mitochondria confers sensitivity to methomyl and to Texas-cytoplasm-specific fungal toxins.
- Mutator-Induced Mutations of the Rf1 Nuclear Fertility Restorer of T-Cytoplasm Maize Alter the Accumulation of T-Urf13 Mitochondrial Transcripts
- Fungal toxins bind to the URF13 protein in maize mitochondria and Escherichia coli.
- Rf8 and Rf* Mediate Unique T-Urf13-Transcript Accumulation, Revealing a Conserved Motif Associated with RNA Processing and Restoration of Pollen Fertility in T-Cytoplasm Maize