Australia - Making sense of varietal responses to new rust pathotypes

A cereal variety is a package of genes. Some genes control yield, some control quality, and so on. There are also genes that control resistance to pests and diseases – the so-called resistance genes.

Rust resistance genes in wheat that have been genetically characterised are catalogued and numbered, with the prefix Yr, Lr or Sr depending on whether they give resistance to stripe rust, leaf rust or stem rust, respectively.

It is sometimes said that a variety does not carry any rust resistance gene at all, but in reality what is actually meant is that the variety does not carry any resistance gene that provides protection against the rust pathotypes it has been exposed to.

It is entirely possible, and is usually the case, that a rust-susceptible variety does carry one or more resistance genes, but that the genes present are ineffective in protecting against the rust pathotypes that prevail in a region.

Knowing the presence of resistance genes in a variety – both those that are effective and ineffective against current pathotypes – is important in predicting and explaining how a variety will perform if and when a new rust pathotype appears. This is well illustrated by the events that unfolded following the introduction of wheat stripe rust pathotype 198 E16 A+ J+ T+ 17+ (198) in 2018, which originated from either Europe or South America.

Knowing the presence of resistance genes in a grain variety is important in predicting and explaining how a variety will perform if and when a new rust pathotype appears.
Photo: Nicole Baxter

Arrival of 198

As is often the case, some wheat varieties were rendered susceptible following the arrival of 198. For example, several durum wheats that carry the resistance gene Yr56 experienced increased stripe rust infection because 198 overcomes this gene, causing rust symptoms to develop.

However, some wheat varieties that were susceptible to the stripe rust pathotypes that prevailed before 2018 proved to be resistant to 198. Our research determined that this was due to the presence of the resistance gene Yr25 (for example, DS Pascal , RockStar and Scepter ). In several other varieties that were previously susceptible, but proved resistant to 198, we discovered they carried a resistance gene that had never been found before (for example, DS Faraday and Elmore CL Plus ).

Identifying these two resistance genes and the varieties that carried them was crucial in explaining the change in stripe rust responses that followed the introduction of 198 in 2018.

We call genes like those found following the introduction of 198 "fossil" genes, because they are hidden in the wheat genome and are only revealed when a pathotype with matching resistance appears.

While the appearance and increase in frequency of a new rust pathotype could result in a variety being rendered more susceptible, it can also result in another variety being rendered more resistant.

Despite being broadly ineffective, fossil resistance genes can assume importance in protecting against rust following a major shift in the composition of a rust pathogen population. Another example of a fossil gene is the leaf rust resistance gene we identified and named Lr82.

Present in Espada , Impose CL Plus, Tungsten and Wedin, this gene was completely useless before 2008 because all leaf rust pathotypes that occurred before then were virulent for it. Our detection of two exotic leaf rust pathotypes unable to overcome Lr82, one in 2005 and one in 2014, and their subsequent build-up in the leaf rust pathogen population in Australia, has meant that for the past 10 years Lr82 has provided very good protection against leaf rust across Australia.

An important lesson from this is that while the appearance and increase in frequency of a new rust pathotype could result in a variety being rendered more susceptible, it can also result in another variety being rendered more resistant.

Resolving these situations is critical in accounting for changes in the responses of varieties that follow changes in rust pathogen populations, and in predicting what will likely happen in the future so that resistance breeding can be tailored to take this into account.

This can only occur by close monitoring of rust pathogen populations for change, and equally importantly using this information to understand the resistance genes present in varieties – both effective and ineffective.