Not only is nuclear DNA vulnerable to mutations but also that in mitochondria. One of the dramatic examples was the occurrence of sterile cytoplasm in corn. And the unexpected variant in a pathogen that attacked the variant mitochondria. Below is a post from 7/27/2017.
MITOCHONDRIAL DNA, CORN MALE STERILITY AND RACE T
All living cells of plants and animals have mitochondria, organelles that convert carbohydrates into the useful form of energy that drives synthesis of metabolites in cells. Mitochondria are believed to be descendants of bacteria that became symbiotic with cells in the early evolution of most living forms. They retained their own DNA, are transferred to the next generation only in eggs cell and not sperm. They replicate within cells but the host cells have some control on the rate of replication. Energy conversion in mitochondria occurs on their folded membranes in a series of chemical reactions. Regions of the plant undergoing rapid cell duplication have more mitochondria. This includes the tassel cells of a corn plant. The pollen mother cells in that region undergo meiosis and duplication, driven partly by the energy conversion by concentration of mitochondria in those mother cells.
A small defect in mitochondrial DNA of an inbred caused a defective membrane product in those mitochondria resulting in incomplete development of pollen. This was found in a corn breeding program in Texas. As the inheritance of this condition was known to be only transmitted independent of nuclear DNA, it was called Texas male sterile cytoplasm. It became a useful tool to corn hybrid seed production because it was easily transferred in breeding programs to the female parent of a hybrid, and thus avoiding manual removal of tassels in seed production fields. Use of T male-sterile cytoplasm became common in the worldwide corn in the 1960’s.
It was noted in the Philippines in 1961, that a fungal pathogen, then known as Helminthosporium maydis, was especially aggressive on several hybrids with T cytoplasm. Despite a few scattered reports elsewhere it was not until 1969 that the connection between increased occurrence of this disease and T cytoplasm became alarming. Majority of seed produced for 1970 corn season had T cytoplasm, the main exceptions being new hybrids in which the conversion to sterility of the female parents was incomplete.
Although the pathogen was normally found in the southern half of the corn belt, and adequately controlled by products of nuclear DNA genes, this disease was found highly destructive in northern corn belt areas as well. A race of the fungus (now named Bipolaris maydis and by its sexual stage Cochliobolus heterostrophus) called race T, produces a toxin that causes death to cells with mitochondria having the DNA with the defect associated with T male sterility. All cells of the corn plant with these defective mitochondria were vulnerable to the fungus. This included the cells in developing seed resulting in diseased stored grain as well as overwintering leaves and stalks. Normal resistance mechanisms to the pathogen were ineffective because the toxin destroyed these defective mitochondria.
As the relationship with T cytoplasm was realized, seed companies worked to change, and within a few years, the disease subsided back to its normal distribution. It was a new learning experience of interaction of corn and pathogen biology.
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About Corn Journal
The purpose of this blog is to share perspectives of the biology of corn, its seed and diseases in a mix of technical and not so technical terms with all who are interested in this major crop. With more technical references to any of the topics easily available on the web with a search of key words, the blog will rarely cite references but will attempt to be accurate. Comments are welcome but will be screened before publishing. Comments and questions directed to the author by emails are encouraged.