The problem with agriculture
A typical wheat field is a monoculture, composed of plants that are clones. These clones all grow at the same rate and set seed at the same time, which makes the decision on when to harvest easy. This convenience comes at a high cost. The uniformity of the plants make the entire field vulnerable and a field epidemic rapidly spreads its disease to neighbouring fields. Pathogens evolve mechanisms to attack plants and acquire nutrients from them. Once established, these mechanisms are easily shared within a pathogen species through sexual recombination. A more interesting form of evolution occurs when pathogens exchange DNA between species; a biological process known as Horizontal Gene Transfer (HGT). We observe HGT events by detecting genes or sequences of DNA that are near identical between distantly related species. To an untrained eye, it may appear that these DNA fragments are “copy-and-pasting” themselves between organisms. My work investigates one of these cases, where a single horizontally transferred gene that confers extreme virulence towards wheat, is shared between three fungal species.
ToxA, a selfish gene that kills wheat
I utilise whole genome sequencing to understand how fungal pathogens interact with plants. We have known for some time that the wheat toxin ToxA is produced by two fungal wheat pathogens, Parastagonospora nodorum and Pyrenophora tritici-repentis. These pathogens are hypothesized to have shared ToxA and some surrounding DNA with each other via HGT, resulting in an 11 thousand base sequence that is near identical between the two species. In our study, genome sequencing unexpectedly revealed the presence of ToxA in the genome of the fungal wheat and barley pathogen Bipolaris sorokiniana. Remarkably, ToxA found in our genome assembly has the exact same 11 thousand base fragment that is found in the other two species, with near identical DNA sequence. The high identity shared between these three species indicates that this HGT event must be extremely recent, perhaps occurring within this century. It also demonstrates the value of ToxA itself, which is important enough to be shared between three separate wheat diseases.
We know that ToxA is responsible for necrosis (cell death) on the wheat leaf during infection. It does this in a very specific way by acting in a ‘gene-for-gene’ relationship with a wheat susceptibility gene, Tsn1. If both genes are present, ToxA in the fungus and Tsn1 in wheat, the infected leaf dies. If either gene is absent, then there are no ToxA related symptoms. We tested whether our B. sorokiniana isolates carrying ToxA had higher disease symptoms on wheat varieties that contain Tsn1. Our results unequivocally showed that a B. sorokiniana isolate carrying ToxA has increased leaf necrosis on Tsn1 wheat in comparison to a non-Tsn1 wheat variety. This is important for two reasons: (1) It shows that ToxA plays a critical role in the disease caused by B. sorokiniana (2) There are other unknown virulence factors in B. sorokiniana that damage wheat in the absence of ToxA.