ARS | Publication request: Gene Silencing Indicates a Role for Potato Endoglucanase Inhibitor Protein in Germplasm Resistance to Late Blight

Submitted to: American Journal of Potato Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: August 11, 2005
Publication Date: October 13, 2005
Citation: Jones, R.W., Ospina-Giraldo, M., Deahl, K. 2006. Gene silencing indicates a role for potato endoglucanase inhibitor protein in germplasm resistance to late blight. American Journal of Potato Research 83:41-46.

Interpretive Summary: Late blight disease can destroy potato crops. A few types of potato have resistance to this disease, but the mechanism of resistance is not understood. We have used a method of turning genes off in a plant to see what happens to the plant. Turning off a gene for a protein that blocks a pathogen enzyme resulted in greater susceptibility to disease. This indicates that the gene is normally beneficial to the plant in conferring disease resistance. This information will be useful to scientists as they develop disease resistant potato plants through either breeding or genetic engineering.

Technical Abstract: Durable resistance to late blight is believed to be dependent on genes other than R genes. Reduced rates of lesion expansion, as found in the germplasm B 0767-2, can provide durable resistance by limiting tissue damage and reducing pathogen populations. We have tested the role of the proteinaceous xyloglucan-specific endoglucanase inhibitor (XEIP) in limiting late blight lesion expansion in B 0767-2. Plant material was silenced for the XEIP using localized infiltration of Agrobacterium tumefaciens harboring pCAMBIA 1302 . Plant cell transformations with pCAMBIA 1302 containing an antisense copy of the XEIP induced effective silencing as indicated by a reduction of up to 80% in XEIP transcript levels. Silencing of XEIP resulted in a marked increase in lesion size and watersoaking, indicating that the inhibitor protein plays a role in limiting lesion expansion in B 0767-2.