The research team at CCDM is made up of scientists specialising in molecular biology, plant pathology, genetics and bioinformatics. The team, in collaboration with other research centres in Queensland and the US*, have been studying the genomes – or complete DNA sets – of NFNB and SFNB to gain a better understanding of their make-up and insight into how the single species net blotch (or in scientific terms Pyrenophora teres) has evolved into two different ‘forms’, causing double-the-trouble.
The answer it seems is partly in the history and partly in something we call ‘host-jumping’!
So, let’s look at the ‘jumping’ first.
Disease outbreaks in humans and animals are often triggered when an infectious agent (such as fungi, bacteria or a virus) suddenly acquires the ability to ‘jump’ across and infect a new host. The same potential for ‘host-jumps’ exists in plant pathogens.
When a host jump happens, a pathogen can suddenly find itself among a lavish monoculture (or entire crop) of susceptible new hosts. The disease can spread, multiply and specialise. Before you know it, there’s a whole bundle of problems!
The CCDM team recently published a paper that provides not only some important genomic tools for further analysis of the disease, but also some new insight into how a pathogen genome changes after jumping into a new crop host.
Net blotch is a disease that presents on the leaf in one of two forms – the NFNB (caused by the pathogen P. teres f. teres (PTT)) and the SFNB (caused by P. teres f. maculata (PTM)).
The two forms are each caused by a specific type of fungus. The two types of fungi are closely related (they both belong to the same species), but they also have their characteristics and differences that make for some compelling research.
The most obvious difference are the different lesions on infected barley.
The net form of net blotch (NFNB) can be identified by lesions that run along leaf veins.
Spot form of net blotch (SFNB) produces round lesions that spread evenly and seem to pay no attention to the longitudinal structure of the leaf.
Then there’s the historical factor – once again offering up some similarities as well as some notable differences.
The similarity is that they are closely related. The two forms parted ways many thousands of years ago, which seems like a long time to us, but is relatively recent in the fungal world! The difference is what they’ve been doing since.
It seems the pathogen that causes NFNB has been a problem for barley growers for at least as long as we have had written records, while the pathogen responsible for SFNB only emerged as a problem on barley in the last 50 or so years.
Essentially one is an ‘ancient’ pathogen while the other is one of those ‘johnny-come-lately’ types!
It’s likely the spot form of net blotch pathogen spent the intervening time living on another host, probably a wild grass, before making the ‘jump’ across to join its ‘relative’ in causing damage in barley.
Comparing the genomes of both pathogens is an important process in better understanding the make-up of both and how we deal with them.
Our researchers can look at what happens to the genome of a pathogen that has lived so long on a crop like barley and how that history affects the genetic arsenal the pathogen brings to bear against its host.
By sequencing and analysing several genomes, our researchers have found that while most of the genome associated with spot form of net blotch (SFNB) is long stretches of genes without much interruption, the net form of net blotch (NFNB) pathogen has a genome ‘fissured’ into islands of genes separated by stretches of repetitive DNA.
The process of breaking the genome into sections seems to be associated with building a more complicated genetic interaction between pathogen and host, leading to the PTM or spot form pathogen having relatively fewer genes associated with pathogenicity whereby PTT or net form seems to have an expanded set.
In other words, in the thousands of years spent infecting barley, the net form pathogen has expanded and refined its molecular arsenal making it a tougher, more virulent force than the ‘younger’ form.
The pathogen responsible for spot form hasn’t had the time to develop the varied molecular arsenal we see in its ‘relative’, and so may be an easier target when developing net-spot resistant barley.
Our researchers also now have access to a panel of high-quality genome assemblies for both pathogen forms, enabling them to further hone in on, understand, and defend against their genetic arsenal.
Through further research they now hope to identify the genes responsible for the net form of net blotch pathogen’s virulence, and provide new information that could potentially be used by breeders to reduce the impact of net blotch in either form.
If you feel like swotting up on more of this important research you can find the full CCDM research paper “Transposable Element Genomic Fissuring in Pyrenophora teres Is Associated With Genome Expansion and Dynamics of Host–Pathogen Genetic Interactions”, published in the journal Frontiers in Genetics, on their website.
