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Two cereal killers conspire against the grain

Earlier in the 20th Century, Septoria Nodorum Blotch was out killing wheat cells on a normal wheat leaf, minding his own business, when Yellow Spot approached him.

“What’s your secret Septoria Nodorum Blotch? Why are you so good at killing wheat cells?” Yellow Spot asked.

“I’ve got this gene called ToxA. It’s amazing – I can kill nearly any wheat cell I want to with it. Do you want to try it?” Septoria Nodorum Blotch said.

“Sure. Pass it over.”

And in that moment, the ToxA gene jumped from Septoria Nodorum Blotch over to Yellow Spot.*

“Wow – I’m way more infectious than ever before!”

Ever since that moment, Yellow Spot and Septoria Nodorum Blotch have infected wheat crops with the ToxA gene, the most potent disease-causing gene in their genomes.

Back at the Centre for Crop and Disease Management, Dr James Hane is looking at all kinds of genomes, trying to find genes like ToxA that have “jumped” or in other words have laterally-transferred from one species to another.

“The vast majority of genes are inherited vertically, that is, they are passed down from parent to child,” James said.

“However very occasionally and especially in microbes, genes can “jump” across vast evolutionary distances – which is referred to as lateral gene transfer.”

According to James, lateral-transfers may hold clues to genes that help the pathogen to survive under stress, evolve and cause disease.

“We are comparing thousands of genomes in a large-scale evolutionary analysis to narrow down where genes have laterally transferred or “jumped” between species.”


toxA jumps


Using ‘Big Data’ approaches to do the comparisons

With the help of supercomputing resources, Dr Hane is currently searching a database of more than 3500 species, including fungi, bacteria, archaeobacteria, oomycetes, insects, plants and algae.

This process is computationally intense, as all of the genes from each species need to be compared to all of the genes in all other species, resulting in over 12 million comparisons, each with about 10,000 to 20,000 genes each.

“Genome sequencing and comparative genomics have come a long way, only 10 years ago we were working with just a handful of fungal species with whole genomes, now there are hundreds,” Dr Hane says.

“We’ve moved our studies from working on a single reference genome for a single species, to comparing hundreds of genomes of the same species or closely-related species – with the increase in scale yielding new insights and improved accuracy.”

Laterally transferred genes are now being analysed

In an initial analysis of just 200 species, James was able to narrow down a number of genes that were laterally transferred some time in history from one species to another and have properties similar to other disease-causing genes.

“These genes have been passed on to CCDM scientists for lab-testing to confirm their role in causing wheat disease,” James said.

“This initial study is only the beginning of what we may find. From the much larger analysis of 3500 species, we’re expecting really good results from a larger and wider survey, including more distantly-related species.”


A circos plot of a whole fungal genome depicting the proportion of DNA sequence occupied by genes (in blue) and various other features. James Hane and his team are comparing 3500 genomes like this one to discover genes that have “jumped” across distantly-related species.


Finding disease-causing genes in fungi helps us to find disease-sensitive genes in crops

Key disease-causing genes in yellow spot or SNB can interact with corresponding sensitivity genes in wheat.

Our mission is to find these disease-causing genes (which produce phytotoxins that we call effectors), as we work on the model that a grain variety insensitive to all effectors will be extremely resistant to a given disease.

Once we find an effector, we can test it on its own against a wheat mapping population and use genetic analysis to determine the approximate location of its corresponding sensitivity gene in the wheat genome.

With this information breeders can go ahead and “breed out” that part of the wheat genome. This will ensure that new wheat lines are insensitive to that effector.

Most commercially-grown wheat varieties no longer carry the wheat sensitivity gene that interacts with the fungal effector ToxA. This gene, we call Tsn1, was swiftly bred out of many varieties as soon as it was discovered a few years ago.

Since then, we’ve seen a significant increase in disease resistance in wheat to both yellow spot and SNB, which has saved Australian growers millions of dollars.


wheat disease duo

Lesions of yellow spot (left) and SNB (right)


About James HaneJames

James joined the CCDM upon its establishment in 2014, leading the bioinformatics research program.

James’ research includes genome analysis of agriculturally-important fungal pathogens and host crop species, and bioinformatic investigation of their interaction during infection.

James also supervises a number of PhD students in bioinformatics, genome analysis and developing novel techniques for predicting pathogenicity genes.

Get in touch with James at


*From paper: Friesen, T. L., E. H. Stukenbrock, Z. Liu, S. W. Meinhardtb, H. Ling, J. D. Faris, J. B. Rasmussen, P. S. Solomon, B. A. McDonald, and R. P. Oliver. 2006.“Emergence of a new disease as a result of interspecific virulence gene transfer.”Nature Genetics 38 (8): 953-956.


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