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ARS Home » Northeast Area » Beltsville, Maryland (BARC) » Beltsville Agricultural Research Center » Genetic Improvement for Fruits & Vegetables Laboratory » Research » Publications at this Location » Publication #357777

Research Project: Potato and Other Solanaceous Crop Improvement and Disease Management

Location: Genetic Improvement for Fruits & Vegetables Laboratory

Title: Assessing possible mechanisms of resistance to early blight caused by Alternaria solani

item Jones, Richard
item Perez, Frances

Submitted to: Potato Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/8/2019
Publication Date: 4/16/2019
Citation: Jones, R.W., Perez, F.G. 2019. Assessing possible mechanisms of resistance to early blight caused by Alternaria solani. Potato Research.

Interpretive Summary: Potato production is often limited by diseases that can reduce growth of the plants or kill them. Fungicides are widely used in an attempt to control potato diseases, however this adds to the costs of production, may cause environmental damage and can be overcome when fungicide resistance occurs. Natural genetic resistance to diseases can be found in wild plant relatives and introduced to cultivated potatoes through breeding or other methods. Understanding what genes are responsible for disease resistance allows for faster incorporation into highly productive cultivated potatoes. We have looked at various genes that may be responsible for disease resistance, comparing susceptible and resistant plants. Certain genes were identified and further tested by transfer to a cultivated variety. One gene was found to be useful in limiting an important disease of potato. This information will be useful in breeding programs, were the gene can be transferred to new potato varieties.

Technical Abstract: Early blight, caused principally by Alternaria solani, is one of the most important foliar diseases of potato, second only to late blight, caused by Phytophthora infestans. Infections generally occur on older tissue first, but can infect any age tissue. Fungicide applications are the principal method for early blight management. Understanding the mechanisms of resistance in potato germplasm can provide direction for breeding efforts aimed at controlling early blight. While late blight can be controlled by deployment of R genes, there are no specific R genes identified for control of early blight, suggesting reliance on multigenic traits. Candidate genes that may be involved in resistance were selected based on toxin resistance (Asc1 and metallothionein), pathogen recognition and response (ACRE-like, Pr5 and RhoB), and reduced cell death (Bax I). Gene expression levels of two early blight resistant breeding line diploids BD-1235 and BD-1265, along with a resistant wild potato, S. raphanifolium were compared to two early blight susceptible diploids, BD-1214 and BD-1217, at 18 hrs after inoculation with Alternaria solani. The largest change in gene expression was seen with the ACRE-like gene, a chitin responsive ubiquitin ligase, where all lines showed increases. The Asc1 gene was found to encode the toxin resistant form in both susceptible and resistant lines. Expression levels increased in two resistant lines and one susceptible line, but was not expressed in S. raphanifolium. Both Pr5 and RhoB expression levels were low in all lines. Expression of two genes (metallothionein and Bax I) diverged, being down-regulated in BD-1235 and upregulated in BD-1265 and/or S. raphanifolium, suggesting differences in resistance response between resistant lines. To determine how gene expression correlates with resistance responses, functional gene analysis was performed through development of transgenic Bintje potato plants with constitutive overexpression of metallothionein or Bax I. There was no significant change in disease observed in detached leaflets of metallothionein transgenics while Bax I transgenics showed a reduction in lesion size and halo formation. Differences in resistance between the two sets of transgenic plants supports the need to pair gene expression with functional analysis to properly determine resistance mechanisms.