Key points
- Two PhD candidates at Griffith University are researching whether chickpea could ignore a ‘special ambassador’ sent by the fungus Ascochyta rabiei
- If so, they could withstand the subsequent invasion of Ascochyta blight
- They are exploring this possibility using new technologies
Ahead of the potential invasion of a chickpea crop, the fungus Ascochyta rabiei sends out a special envoy of proteins.
Called ‘transcribed and secreted effector molecules’, these proteins enter chickpea cells and manipulate their functions, helping A. rabiei to survive in the plant and allow the disease Ascochyta blight to take hold.
However, this incursion can only occur if the chickpea host recognises the fungus. If chickpeas do not recognise and react to these proteins, plants could be bred to withstand the fungal invasion. Two PhD candidates at Griffith University are researching this potential.
Mahmuda Binte Monsur and Matin Ghaheri are working with Professor Rebecca Ford and Dr Ido Bar on a GRDC-supported project to explore the molecular drivers behind pathogenicity with new technologies.
Ms Monsur says determining which fungal proteins are involved creates the potential to breed plants that do not recognise them – in effect saying: “a true host has not been found. Do not invade”.
“Ultimately, by blocking the interaction between A. rabiei effectors and chickpea cells, it could be possible to reduce the severity of Ascochyta blight disease and improve crop yield and quality.”
Molecular study
Ms Monsur has identified a suite of molecules (called putative effectors) that are produced by A. rabiei and which are suspected of playing a role in causing plant disease.
“These molecules have been identified based on their genetic sequences and by using bioinformatic tools,” she explains. “But their exact functions are not yet known.”
“Bioinformatic approaches help us understand which genes are actively involved in the pathogenicity (the property causing disease) by comparing the genetic makeup of highly aggressive and less aggressive isolates.”
Meanwhile, Ms Ghaheri is investigating how the A. rabiei effector molecules are packaged and transported to enable direct contact and interaction with the host chickpea cells.
She is doing this by studying transport mechanisms – the nanoparticles (called extracellular vesicles) that move DNA, RNA, proteins and lipids to locations within and between organisms.
One type of extracellular vesicle is already associated with invading organisms. Using bioinformatic analysis, it has been found to contain pathogenic-related proteins.
The PhD students’ supervisor, Professor Ford, says the molecular work is important. Ascochyta blight disease of chickpeas, caused by A. rabiei, represents a significant threat to chickpea production globally.
“Understanding the molecular mechanisms underlying A. rabiei pathogenicity is crucial for developing effective strategies to mitigate the impact of this damaging disease.”
Ascochyta blight is currently estimated to, on average, be reducing chickpea yields by up to 20 per cent a year.
More information: The Current and Potential Costs from Diseases of Pulse Crops in Australia