Submitted to: Advances in Agronomy
Publication Type: Review Article
Publication Acceptance Date: 3/31/1998
Publication Date: N/A
Citation: N/A Interpretive Summary:
Technical Abstract: Cytoplasmic male sterility (cms) systems have been identified in over 150 plant species and have been exploited in the breeding of a number of crops. The Texas or T-cytoplasmic male-sterile (cms-T) system was used extensively in the 1960s to eliminate the need for hand detasseling in the production of hybrid maize seed. However, in 1970, T-cytoplasm maize succumbed to a severe epidemic of southern corn leaf blight. As a consequence of this epidemic, cms-T is no longer widely used commercially. However, it has been developed as a model system to study mechanisms underlying disease susceptibility, male sterility, and fertility restoration. T-cytoplasm maize is acutely sensitive to host-selective toxins (T-toxin and PM-toxin) produced by two fungi, race T of Cochliobolus heterostrophus and Mycosphaerella zeae-maydis, respectively. Both male sterility and toxin sensitivity are due to the action of a chimeric mitochondrial gene, T- urf13, which encodes a 13-kD inner-mitochondrial-membrane protein. Although it is known that, following infection, T-toxin binds to the URF13 protein and thereby permeabilizes the mitochondrial membrane resulting in cell death, the mechanism by which T-urf13 causes male sterility is still not clear. Full or partial fertility restoration of T-cytoplasm maize is mediated by the Rf2 nuclear restorer, in combination with one of three other restorers: Rf1, Rf8, or Rf*. Rf2 encodes a protein highly similar to mitochondrial aldehyde dehydrogenases; Rf1, Rf8, and Rf* each mediate discrete T-urf13 mitochondrial transcript processing events. These advances have laid a foundation for determining mechanisms of male sterility and fertility restoration in the T-cytoplasm male-sterility system.