Nuclear-mediated mitochondrial gene regulation and male fertility in higher plants: Light at the end of the tunnel?
- Roger P. Wise†,‡ and
- Daryl R. Pring§
- †U.S. Department of Agriculture–Agricultural Research Service, Corn Insects and Crop Genetics Unit, Department of Plant Pathology, Iowa State University, Ames, IA 50011; and§ U.S. Department of Agriculture–Agricultural Research Service, Crop Genetics and Environment Unit, Department of Plant Pathology, University of Florida, Gainesville, FL 32611
Hybrid vigor, or heterosis, in higher plants is often attained through the use of cytoplasmic male sterility (CMS), a maternally inherited trait characterized by the absence of functional pollen. Hybrids of many plants are produced using CMS, wherein a male-sterile line is grown adjacent to a selected male-fertile line, which functions as a pollen source. Seed formed on the male-sterile line is then grown as a hybrid. When the hybrid plant is harvested for its vegetative parts, sugarbeet for instance, it is immaterial that the F1 hybrid is male-sterile. However, in plants where the seed is harvested, it is imperative that the F1 hybrid be male-fertile. Fundamental characteristics of CMS impact on this consideration. Historically, most sources of CMS were discovered as a result of genetic crosses involving normal, male-fertile plants, wherein male-sterile plants were observed among the progeny. Lines that allow male sterility to be expressed were thus identified as potentially useful for plant breeding. It is this fact that enables the utilization of CMS: some lines allow CMS to be expressed and some do not.
How then can the molecular identity of Petunia Rf be reconciled with its known effect on the pcf transcript or its encoded mitochondrial protein?
CMS systems are found in over 150 plant species and are usually attributed to chimeric ORFs in the mitochondrial genome. These ORFs encode novel proteins, which often interfere with mitochondrial function and pollen development. Evolution has provided the answer to these aberrant mitochondrial proteins through nuclear-encoded, restoration of fertility, or Rf, genes, which suppress mitochondrial abnormalities associated with male sterility. This suppression allows normal metabolic processes that lead to successful microsporogenesis. In many instances, this suppression is directly associated with Rf-gene-dependent, mitochondrial RNA modification and concurrent reduction of the CMS-associated protein (1). Although many mitochondrial …
