Alumni Memories

Essays on the College of Agriculture's History

Looking back at nearly 50 years at Iowa State

by Charlie Martinson, emeritus professor

Charlie Martinson,
emeritus professor

Editor’s note: Charlie Martinson served Iowa State University for 30 years as a faculty member of the plant pathology department from 1968-1998. Martinson shares his experiences with the Southern corn leaf blight pandemic and the steps taken to stop it from spreading further.

A flash back of 37 years to 1970 returns one to a plant disease pandemic that would bring plant pathology to the limelight and Southern corn leaf blight would be the topic of nearly every newscast and conversation in local cafes. From late July through about August 9, the aftermaths of tropical storm Becky and hurricane Celia locked the Corn Belt and much of Iowa into weather characteristic of the lowland tropics.

Temperatures hovered in the mid to high 80s for much of the day and persistent sometimes heavy rains prevailed so that leaves remained moist almost continuously. These were ideal tropical conditions for the Southern corn leaf blight fungus, Helminthosporium maydis, to produce thousands of spores in isolated necrotic lesions on corn leaves. Splashing rain and turbulent wind spread these spores to new leaves, plants, and fields where in 60 hours a new lesion about one inch long would form and be producing thousands of additional spores. The extended warmth and humidity allowed numerous cycles of infection of vulnerable leaves, ears and husks by H. maydis.

Eastern Iowa, which was exposed to record levels of rainfall in August and September, suffered the greatest with yield losses of 30 to 70 percent or more while western Iowa escaped much of the disease epidemic. The Southern corn leaf blight epidemic occurred from Florida up to the Mid-Atlantic States and west to Iowa, Minnesota, Missouri and Texas. Some farmers in the southern United States had total losses. Yet, about 15 percent of the cornfields in heavily diseased areas remained relatively disease free.

A year earlier, in the fall of 1969, I observed Southern corn leaf blight attacking corn ears and rotting the kernels and by working with the seed companies we discovered that corn containing Texas male sterile cytoplasm was very susceptible, whereas normal cytoplasm corn was resistant to the disease. It was found that a new race of H. maydis was involved and it produced a host specific toxin that was toxic only to corn with Texas male sterile cytoplasm, now known as Tcms.

Tcms is maternally inherited and is passed from one generation to the next through the cytoplasm. Pollen from another plant was needed for fertilization and seed produced from the plant would carry the Tcms trait. Nuclear inherited genes would restore fertility (Rf) to Tcms. Seed corn companies capitalized on Tcms to save detasseling costs. Their inbred lines used to make hybrid crosses were backcrossed into Tcms plants which would become the seed parents for hybrid seed production and the Rf gene was bred into the pollen parent for the hybrid cross. In the farmer’s field the hybrid variety would be male fertile and produce pollen although the cytoplasm still carried the Tcms gene and susceptibility to the toxin. Tcms technology eliminated most of the labor with hybrid seed corn production, but it created cytoplasmic uniformity; in 1970 about 85 percent of the corn plants in the United States could be maternally traced back to one corn plant discovered in Texas in 1944.

Much of the seed produced in 1969 for the 1970 crop was found by the Iowa State University Seed Laboratory to contain kernels infected with H. maydis, which we found would kill the young seedlings and sporulate on the killed tissue. ISU Extension pathologists warned Iowa farmers to avoid seed with Tcms, but this caused a backlash by many of the seed companies who were unaware of the potential dilemma.

Reports of Southern corn leaf blight epidemics came in from Southern states prior to the epidemic to hit the Corn Belt. We observed isolated lesions of the disease on plants soon after emergence, but the disease never developed beyond a few lesions per plant because we were in a rather dry growing season. Then when the hot humid weather came and persisted, the epidemic exploded. Corn futures shot upward and the ISU corn pathologists spent more time answering phone calls and doing TV, radio and press interviews than they did studying the disease epidemic.

Floyd Andre, dean of the College of Agriculture, recognized the chaos of the situation, especially with the commodity markets, and established a corn blight information committee that would make all news releases from ISU and these were to be made every Friday after the Chicago Commodity Markets closed. Scientists involved could not invest in commodity futures. Other states did not follow Iowa’s lead in 1970, but federal regulations required them to follow the Iowa protocol in subsequent years.

After the 1970 harvest season, local corn prices increased 70-90 percent above those prior to the epidemic and those farmers with little to moderate levels of disease experienced an economic windfall. For some it was a disaster, even with the higher prices. I lead the charge, with scientists at seven other state experiment stations, to seek a special appropriation from Congress for research on Southern corn leaf blight, H. maydis, and how we might avoid another epidemic like 1970. This was the first time agricultural scientists had ever gone to Congress directly and Congress was very receptive. We asked for $4 million and got $2 million with a stipulation from Jaime Whitten, chair of the House Agriculture Appropriations committee, that Mississippi State University (in his constituency) also got an equal share of the appropriation.

Even split nine ways, this adequately funded a broad cooperative research endeavor among the nine states. At ISU, I was funded in plant pathology and studied chemical control, the physiology and cytology of the host specific toxin in corn, and the development of a relatively rapid assay using the toxin to test for Tcms in plants, which was used to screen hundreds of thousands of Tcms plants to see if separation of toxin susceptibility and male sterility might occur (it did not). The assay was adopted by numerous seed companies (we provided the toxin for free) to screen their normal cytoplasm seed stocks for contamination by Tcms. The grant also supported Harry Horner in botany who studied the cytology of male sterility, Carl Tipton in biochemistry who studied the nature of the host specific toxin, Peter Peterson in agronomy who studied the genetics of the system, and several post-doctorates and graduate students.

The outlook for corn production in 1971 was questionable. Seed companies produced some normal cytoplasm seed in Hawaii and the southern hemisphere and imported some from Hungary and Yugoslavia, but about 50 percent of the seed contained Tcms and was contaminated with race T of H. maydis. Early season lesions developed, but the weather was drier and much cooler than in 1970 throughout most of the Corn Belt; no epidemic developed and by 1972 all of the seed was resistant to race T of H. maydis.