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AGWEEK

Silver scurf, caused by a fungus, is a common potato disease and found in all major production areas of the U.S., including the Red River Valley of western Minnesota and northeast North Dakota.(Photo by Andrew Robinson)

Silver scurf: Great name, but bad for spuds

GRAND FORKS, N.D. — Fans of colorful, alliterative language may like “silver scurf.” Not Red River Valley potato growers; they see the crop disease as a growing threat.

“I’m getting more questions about it at harvest,” said Andy Robinson, Fargo, N.D.-based potato extension agronomist for both North Dakota State University and the University of Minnesota.

 He helped to organize potato educational sessions during the recent International Crop Expo in Grand Forks, N.D., and brought in Amanda Gevens to speak on the crop disease on Feb. 22.Gevens, a professor in the plant pathology department at the University of Wisconsin, also is seeing more cases of silver scurf. She described the disease “as gray, silver and shiny patches” that are “more obvious on red and purples,” but seen on yellow and russet potatoes, too.

Silver scurf, caused by a fungus, is a common potato disease and found in all major production areas of the United States, including the Red River Valley of western Minnesota and northeast North Dakota.

 The disease, specific to potato tubers, causes blemishes on spuds. Though the effect is mostly cosmetic, some potatoes affected by the disease have been rejected by industry buyers. Efforts to combat silver scurf are complicated by its close resemblance to black dot, another crop disease. Even Gevens can have trouble distinguishing the two diseases on affected potatoes.

 

“Whodunnit? Is it a silver scurf problem? Or is it a black dot problem,” she said. “It’s hard to tell these apart. Sometimes you can’t tell them apart.”

One important difference: silver scurf is tied to infected seed, while black dot is more of a soil/field debris issue, Gevens said.

 No commercial cultivars resistant to silver scurf are available yet, though work to develop them is underway.

Use of uninfected seed, which can be hard to get, helps to control the disease, as does early harvest and chemical use,

Storage conditions also influence the extent of silver scurf in affected potatoes. “High humidity in storage encourages it,” Gevens said.

Research also shows that smaller storage volumes help to control core temperatures and hold down silver scurf. But limiting storage volumes may not always be feasible, she said.

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Science Daily

 Linking virus sensing with gene expression, a plant immune system course-corrects
Date:
March 6, 2018
Source:
American Society for Biochemistry and Molecular Biology
 
FULL STORY

Plant immune systems, like those of humans and animals, face a difficult balancing act: they must mount responses against ever-evolving pathogens, but they must not overdo it. Immune responses require energy and resources and often involve plants killing their own infected cells to prevent the pathogens from spreading.

Researchers at Durham University in the UK have identified a crucial link in the process of how plants regulate their antiviral responses. The research is published in the March 2 issue of the Journal of Biological Chemistry.

Martin Cann’s lab at Durham, in collaboration with the laboratories of Aska Goverse at Wageningen University and Frank Takken at the University of Amsterdam, studied a receptor protein called Rx1, which is found in potato plants and detects infection by a virus called potato virus X.

Binding to a protein from the virus activates Rx1 and starts a chain of events that results in the plant mounting an immune response. But the exact sequence of cellular events — and how Rx1 activation was translated into action by the rest of the cell — was unknown.

“Our study revealed an exciting, and unexpected, link between pathogen attack and plant DNA,” Cann said.

Specifically, the study showed that Rx1 joins forces with a protein called Glk1. Glk1 is a transcription factor, meaning it binds to specific regions of DNA and activates genes involved in cell death and other plant immune responses. The team found that when Glk1 bound to virus-activated Rx1, it was able to turn on the appropriate defense genes.

Interestingly, when the viral protein was absent, Rx1 seemed to have the opposite effect — actually keeping Glk1 from binding to DNA. In this way, it prevented an inappropriate immune response.

“The immune response involves reprogramming the entire cell and also often the entire plant,” Cann said. “An important part of this regulatory process is not only allowing activation but also making sure the entire system is switched off in the absence of infection.”

As over a third of the annual potential global crop harvest is lost to pathogens and pests, breeding plants with better immune systems is an important challenge. Understanding how this immune system is regulated at the appropriate level of activity gives the researchers more ideas of points in the immune signaling pathway that could targeted to increase the plant’s baseline ability to resist disease.

“To increase (crop) yield, there is an urgent need for new varieties that are resilient to these stresses,” Cann said. “A mechanistic understanding of how plants resist or overcome pathogen attack is crucial to develop new strategies for crop protection.”

Story Source:

Materials provided by American Society for Biochemistry and Molecular Biology. Note: Content may be edited for style and length.


Journal Reference:

  1. Philip D. Townsend, Christopher H. Dixon, Erik J. Slootweg, Octavina C. A. Sukarta, Ally W. H. Yang, Timothy R. Hughes, Gary J. Sharples, Lars-Olof Pålsson, Frank L. W. Takken, Aska Goverse, Martin J. Cann. The intracellular immune receptor Rx1 regulates the DNA-binding activity of a Golden2-like transcription factor. Journal of Biological Chemistry, 2018; 293 (9): 3218 DOI: 10.1074/jbc.RA117.000485

American Society for Biochemistry and Molecular Biology. “Linking virus sensing with gene expression, a plant immune system course-corrects.” ScienceDaily. ScienceDaily, 6 March 2018. <www.sciencedaily.com/releases/2018/03/180306153726.htm>.

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