A mitochondria genetic mutation

​We moved from Tennessee back to the Midwest in August of 1970 with a fresh PhD in Botany with a specialty in Mycology to take a temporary Post Doc position at Illinois State University to study fungi.  I recall seeing corn fields turning brown, thinking that is not consistent with my younger Iowa experience.  It was quickly realized by many others that the early corn death was associated with a race of a relatively moderate corn fungus, Bipolaris(Helminthosporium) maydis, producing a toxin attacking corn leaves.  Susceptible hybrids all had t-cytoplasm.
 
Most genetics in a corn plant are located on chromosomes in the cell nucleus.  A few of the organelles, such as plastids and mitochondria, in cell cytoplasm have their own genetics, consistent with the theory of their ancient derivation from bacteria.  Mitochondria are the site in which carbohydrates are processed to provide energy for all metabolic pathways in living cells.  Mitochondria duplicate and multiply within cells and are generally only passed onto the next generation of an organism through the female ovule, but not the sperm cells.  They accumulate in areas of most cell activity, such as cell division leading to pollen production.  The base cells that undergo meiosis and cell multiplication resulting in corn pollen contain 40 times as many mitochondria as other corn cells.
 
After it was realized that some cytoplasmic genetics would interrupt production of viable pollen, the cytoplasm was crossed into female parents of hybrids to reduce effort and cost of producing hybrid seed.  It is believed that, by 1970, 85% of hybrid corn planted in USA had the T-cytoplasm.  Use of this sterility system was also used extensively in many other countries.
 
The mutant mitochondrial gene (T-urf13) encodes for a protein in the mitochondrial membrane, ultimately disrupting normal mitochondrial function, and thus interfering with production of normal pollen.  It was discovered after the corn disease outbreak that the same membrane defect allows the fungal toxins produced by B. maydis and a much less significant fungus (Mycosphaerella zeae-maydis), cause of yellow leaf blight, to reduce the natural genetic resistance to these pathogens.
 
Full realization of the linkage of disaster associated with t-cytoplasm resulted in urgent winter seed production by all corn seed companies in an attempt to avoid repetition of the problems.  In the 1971 season, I was asked to assist in monitoring the 1971 progress of the disease by Funks G Hybrid company and thus got involved in corn pathology.  I can now claim that a mutation in a corn mitochondrion got me lost in the corn field and that I have yet to find my way out!
 
There are many studies on race t and t-cytoplasm. One is: https://lib.dr.iastate.edu/cgi/viewcontent.cgi?article=1060&context=bot_pubs