Potato blight image

Infected potatoes are shrunken and rotted.

At RIKEN’s Plant Science Center scientists have discovered that a protein released by the potato blight pathogen P. infestans uses a sticky patch of amino acids to adhere to potato plant cells, thereby avoiding immune detection.

Late blight of potato is an economically devastating disease affecting potato farmers all over the world. Potato blight was a major cause in the 1840s European potato famines, and today it is responsible for causing tens of billions of dollars’ worth of damage every year. Phytophthora infestans, the pathogen which causes late blight, continues to thwart eradication efforts. It has evolved to overcome many fungicides and even major resistance genes that have been bred into commercial potatoes.

In order to supress the immune response of its host, P. infestans produces molecules called disease effectors. Scientists in Japan and the UK have determined the molecular structure of the disease effector called ‘avirulence protein 3a’ (AVR3a), which is known to inhibit disease defences in potato plants.

The team used a technique called nuclear magnetic resonance spectroscopy to study the configuration of AVR3a. They identified a patch of positively charged amino acids which is found in all the different versions of AVR3a from P. infestans and another pathogen called P. sojae, indicating that this part of the overall structure could be important to the infection process.

To determine whether the newly identified section of positively charged amino acids is essential for the disease effector to stick to potato cells, the team developed a strain of mutant P.infestans whose AVR3a protein lacked the positively charged patch. They found that without this patch the mutant effectors are unable to attach to the potato cell membrane, which suggests that by binding to the cell membrane AVR3a may help P. infestans evade the potato’s immune system.

Ken Shirasu, one of the researchers involved, says that the next challenge is to determine how AVR3a molecules and other disease effectors from P. infestans get into the host from the site of infection.

“Developing ways to block the action of AVR3a and other disease effectors will provide means to control this damaging crop disease,” he said.

For further information contact:

Dr Ken Shirasu
RIKEN Plant Science Center, Japan
Email: gro-pr@riken.jp