2012 Annual Report
1a.Objectives (from AD-416):
In 2009, a new late blight strain US-22 was identified along the East coast and as far west as Wisconsin. This strain was virulent on potatoes and significantly impacted potato production in affected areas. There was greater variation in the strains identified in potato fields in the U.S. in 2010, however US-22 was again identified in WI along with US-23 and 24. Although not yet present in the USA, destructive and highly virulent strains of P. Infestans have spread through Europe (genotype Blue 13), and are present in Guatemala (currently uncharacterized). These new strains can be much more aggressive compared to the old populations. We need to be prepared with germplasm that is resistant to highly virulent strains.
1. Conduct transformations with candidate sequences of a putative S. microdontum R-gene.
2. Identify functional orthologs of the late blight R-gene RB from disease resistant wild germplasm and test the functionality of these genes using a transient expression assay.
3. Evaluate the late blight resistant potato advanced breeding lines including the varieties 'Defender' and 'Jacqueline Lee' for resistance to Blue 13 and identify the presence of genes that recognize P. infestans effectors.
4. Evaluate the effect of pyramiding the RB with conventionally bred late blight resistant lines.
1b.Approach (from AD-416):
Test the resistance phenotype of transgenic plants with the S. microdontum gene to P. infestans isolates collected from the United States and Guatemala.
We have determined that certain strains of the late blight pathogen can overcome important resistance genes in potato, including the RB gene. Over the past year, we have identified several variants of the RB gene from various wild species of potato in the hopes that one or more of these genes will confer resistance to new pathogen strains. We have determined that a specific region of the RB protein interacts directly with a molecule that is derived from the late blight pathogen. This interaction likely takes place within the host cell cytoplasm and leads to suppression of the RB protein, resulting in susceptibility (disease). We have identified wild species variants of the RB protein that do not interact with this late blight pathogen molecule and we hypothesize that these variants may confer more durable resistance to late blight – even to newly identified virulent strains of late blight. We are currently in the process of engineering RB genes to test this hypothesis.
This research relates to Objective 1, Develop adapted potato clones with enhanced resistance to major potato diseases.