Mitochondria and corn male sterility

Plant and animal cell cytoplasm includes mitochondria and other organelles.  As discussed previously, the mitochondria function as the main source of providing chemical energy to the rest of the cell for growth, cell division and motility.  Mitochondria and chloroplasts also have their own DNA, provide their own division and multiplication and are only transmitted through egg cells in sexual reproduction.  The DNA in these organelles is relatively stable but occasionally have mutations that affect their function.  In many plant species this mutation affects the production of functional pollen.  In these cases, the inheritance being from mitochondria and only occurring in the cytoplasm, the sterility is called cytoplasmic male sterility or CMS.
 
This was discovered in a breeding plot in Texas in the 1950’s when an inbred was found to be male sterile.  It was related to a DNA mutation that affected one of the membrane layers of the mitochondria and the production of a polypeptide (URF13). The result is that the cell divisions needed for pollen production are inhibited.  There are nuclear genes, however, that result in production of proteins that overcome the negative affect of the mitochondria sterility affect and consequently result in production of pollen in a CMS plant.  These are called restorer genes (rf).  The Texas male sterile source (tCMS) was widely used in the 60’s because it allowed seed companies to reduce the expense of hiring people to physically remove tassels on the female parents in hybrid seed production.  The restorer genes were bred into the male parents or the non-sterile versions were mixed with sterile versions in seed sold to farmers so there was adequate pollen for grain production. 
 
In 1969 it was noticed that relatively minor disease in the southeast Corn Belt was suddenly more aggressive. Furthermore, it was much more damaging on plants with tCMS than those without this cytoplasm.  A variant of the fungus Helminthosporium maydis (now Bipolaris maydis) produced a toxin that caused mitochondria with the mutation to swell and destruct. This allowed the fungus to cause large lesions, produce more spores and cause more damage.  Because most of the seed produced in 1969 in the USA had the tCMS mitochondria, most hybrids planted in 1970 was susceptible to this race T of this fungus.  Although seed companies scrambled to build up non-tCMS seed supplies that year and because the August 1970 weather in much of the Midwest had warm humid weather favoring the fungus, grain yield losses approached 40%. 
 
Using southern hemisphere locations, seed companies increased non tCMS parent seed but still managed to only supply blends of tCMS and non CMS seed to farmers in 1971.  Fortunately the August weather in the Midwest that year was more of the drier and cooler night temperatures and the disease damage was limited.  By 1972, the disease was reduced to much more normal levels.