Thoughts on Cytoplasmic Male Sterility in cms-T Maize.

Cytoplasmic male sterility (CMS) is a maternally inherited trait that suppresses the production of viable pollen grains. The Texas, or T, cytoplasm (cms-7) of maize, which was first described in the Golden June line in Texas (Rogers and Edwardson, 1952), carries the CMS trait. The Texas cytoplasm was an important discovery to geneticists and plant breeders because it eliminated the costly detasseling procedure used in maize hybrid seed production. Its commercial value has prompted many applied and basic studies of cms-T aimed at understanding CMS and its relationship with mitochondrial and nuclear genes. Although CMS has been observed in more than 150 plant species (Laser and Lersten, 1972), the mechanism by which it interrupts normal pollen development is not well understood. In this review, the basis of CMS in cms-T maize is considered. In cms-T; male sterility is characterized by the failure of anther exertion and pollen abortion. Female fertility is not affected by CMS, so male-sterile plants can set seed if viable pollen is provided. Comparisons of plants carrying the T and normal cytoplasms reveal very slight differences in severa1 other morphological characters (see below; Duvick, 1965). Initially, the three male-sterile cytoplasms of maize-cms-T, cms-C, and cms-S-were distinguished by specific nuclear genes, termed restorers of fertility (Rf), that suppress the male-sterile effect of the various cytoplasms and allow viable pollen production. For example, two genes, Rf7 and Rf2, acting jointly, restore pollen fertility to cms-7: Rf7 and Rf2do not restore pollen fertility to cms-C or cms-S; instead, different restorer genes are necessary to restore pollen fertility to these cytoplasms. Other characteristics also distinguish male-sterile and normal maize cytoplasms; they include mitochondrial DNA (mtDNA) restriction fragment length polymorphisms, variations in mitochondrial RNA (mtRNA), and differences in mitochondrial translational products (Pring and Levings, 1978; Leaver and Gray, 1982; Newton, 1988). Early on, these distinctions indicated that the various CMS types are based on different mechanisms and hereditary factors. The T cytoplasm is best known for the part it played in the U.S. epidemic of Southern corn leaf blight of 1969 and 1970 (Williams and Levings, 1992). In the two decades before the epidemic, cms-T had replaced detasseling as the chief method of pollen control in hybrid corn production (Wych, 1988), and by 1970, 85010 of the hybrid corn grown in the United States carried the T cytoplasm. After it was determined that cms-T was specifically susceptible to Bipolaris maydis race T, the organism responsible for the blight, its use by the hybrid seed corn industry was largely terminated (Ullstrup, 1972). Phyllosricra maydis, another fungal pathogen, is also specifically virulent on cms-7: Normally, B. maydis race T is a serious pathogen only on maize containing the T cytoplasm. Other male-sterile and normal maize cytoplasms support only limited colonization by the pathogen, and the lesions on the leaves remain small and isolated. By contrast, B. maydis lace T can quickly and completely colonize cms-Tmaize plants, causing extensive plant damage and sometimes death. Susceptibility of cms-Tto B. maydis race T is caused by mitochondrial sensitivity to a host-specific pathotoxin, designated BmT toxin, produced by the pathogen. P maydis also produces a pathotoxin that is structurally similar to the BmT toxin of B. maydis, to which cms-Tmitochondria are sensitive. Accordingly, susceptibility of cms-Tmaize to these fungal pathogens is due to mitochondrial sensitivity to the pathotoxins, whereas disease-resistant maize types have mitochondria that are insensitive to the pathotoxins.