BADGER BEAT

By Dr. Amanda Gevens and Sofía Macchiavelli Giron, University of WisconsinMadison Plant Pathology

to the Badger Common’Tater with a special note about its co-author, now Dr. Sofía Macchiavelli Giron. Sofía recently successfully defended her doctoral dissertation working with me at the University of Wisconsin-Madison Department of Plant Pathology. A summary of some of her results is provided in this article. Many Wisconsin potato growers interacted with Sofía and appreciated her updates on silver scurf and its management at our annual meetings. Further, she was honored, in 2019, with the National Potato Council Scholarship, which enhanced her disease research efforts. I thank our growers and the industry for these collaborative and supportive opportunities for students that help us grow the next generation of agricultural scientists while addressing current crop challenges! Potatoes are the world’s fourthlargest food crop, following rice, wheat and maize. Wisconsin currently

ranks third in potato production in the United States and has been experiencing increased blemish disease incidence and severity since approximately 2000, with a marked impact on quality of fresh market varieties.

continued on pg. 48

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Silver scurf, caused by Helminthosporium solani, is a blemish disease of potato that affects periderm quality and appearance, impacting marketability and storability. Symptoms of the disease include often blotchy, gray, silver or golden lesions on the tuber periderm, depending on variety. The periderm damage caused by this disease can also exacerbate water loss, and hence, yield loss, in storage. Further, the damaged periderm can potentially result in secondary infections by opportunistic pathogens. Most losses associated with silver scurf are due to fresh market rejections or moisture loss from damaged skin. At times, blemish diseases can also cause seed quality downgrades.

The potato silver scurf disease cycle includes infection phases in both the field and storage domains. Infection begins in the field with one or multiple sources of inoculum, including infected seed or soil and/or crop debris. The primary source of inoculum is typically infected seed tubers, although some studies have shown evidence of soil being the main suspect. In recent Central Wisconsin research, molecular biological screening of the soil and plant material within the agro-ecosystem indicated that seed

was the primary source of infection. The fungus can infect developing plant parts (roots and stolons) and ultimately daughter tubers. After harvest, secondary infections can occur in storage through different mechanisms.

Conidia spread by direct contact to other tubers or movement of air through ventilation systems. Planting and harvesting dates are important factors in disease incidence and severity. The length of tuber exposure to H. solani (from tuber initiation to harvest) has been correlated with severity. Studies have shown that later harvest dates lead to higher disease severity. Improved understanding of pathogen source and infection status will help prescribe optimum timing for treatments or cultural practices to further reduce inoculum and disease.

While the host range of H. solani is typically limited to potatoes and solanaceous plant roots, the pathogen can develop mycelial growth, conidiophores and conidia (spores) on alfalfa, sorghum, rye, oats, corn and wheat in senescent tissue after 20 days of incubation in the dark.

In addition, mycelial colonization and sporulation was observed on rapeseed, red clover and buckwheat after five days of incubation on V8 agar.

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There was no colonization present on potato leaves, indicating that, on potatoes, this pathogen is exclusively associated with below-ground plant parts. With limited genetic understanding of, and little commercial resistance to, varietal resistance in potato to silver scurf, producers have had to rely on fungicides and variably effective cultural controls for management of silver scurf and other blemish diseases.

Current management strategies for silver scurf include use of diseasefree seed potatoes; crop rotation of three years or greater for a non-potato crop; mitigation of soil moisture; timing of vine senescence with harvest so that tubers are not left in the soil for two or more weeks after defoliation; and fungicides timed at planting (seed-applied or in-furrow) and post-harvest (in some cases). Fungicide evaluation trials for the control of silver scurf and black dot have resulted in variable outcomes in the past, depending on location, application timing and year. The effectiveness of fungicides at specific times can further inform our understanding of the pathogen’s disease cycle in the field.

Previous studies identified potato breeding clone C287 with resistance to silver scurf. We sought to determine the genetic attributes responsible for this resistance for potential integration into breeding programs to limit disease. C287 was crossed with M6, a diploid self-compatible inbred line of the potato wild relative Solanum chacoense, which is susceptible to silver scurf.

From the progeny, F1-22 was selected, based on disease resistance and tuber type, and self-pollinated to create F2 plants. There were significant differences among F2 clones, including tuber weight and number, indicating that segregation occurred for these traits in this population. Disease symptoms were not visually apparent, so we applied a quantitative PCR approach (a molecular tool to measure how much of the pathogen DNA was present) to quantify pathogen presence. Preliminary results showed variation in resistance between lines. We will use further tests (single nucleotide polymorphisms, or SNP’s) to look for quantitative trait loci associated with silver scurf resistance. This will determine whether a marker for silver scurf resistance can be identified in potato. ii) Fungicide evaluation: In our multiyear investigation, we documented the potato silver scurf control benefits of a season-long integrated approach in Wisconsin.

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