Abstract - Fungal pathogens deploy effector proteins to manipulate host immune responses and facilitate infection. These effectors frequently show discontinuous distributions between species suggestive of horizontal gene transfer (HGT) between species sharing a common host. The effector ToxA of the wheat pathogen Parastagonospora nodorum is a classic example, conveying virulence upon non-pathogenic isolates and notably contributing to the emergence of a new wheat pathogen, Pyrenophora tritici-repentis by means of HGT. Effector genes, such as ToxA, are commonly found in association with transposable elements (TEs) and it has been hypothesised that such elements are a factor contributing to interspecific transfer. However, no specific TE has yet been identified as the unit of transfer in a case of horizontal effector transmission.
Recently, ToxA has been discovered in wheat-infecting isolates of a third species, Bipolaris sorokiniana. Chromosome-level assemblies for multiple B. sorokiniana and P. nodorum isolates enabled us to identify extended regions of shared identity around ToxA. We have subsequently reconstructed a single composite DNA-transposon responsible for mobilising ToxA between species and show this element to be intact and active in B. sorokiniana - this is the first time a functional TE has been definitively linked to a case of HGT in fungi. Further, we find that ToxA resides in a large TE-rich genomic island (syn. AT-isochore or Lineage-Specific region) in all three species. We propose that rare inter-specific hybridisation events facilitate introgression of mobile-element islands into new populations and that these islands act as rafts from which captured effectors may be mobilised.
I have further characterised the role of transposon-directed epigenomic silencing mechanisms is regulating co-located genes. Many fungal plant-pathogens display a rapid shift in gene expression upon infection of a susceptible host. In the wheat-pathogen Parastagonospora nodorum, key necrotrophic effectors, ToxA, Tox1 and Tox3 are strongly induced upon infection and are poorly expressed under in vitro conditions. All three genes are found to occur in close proximity to transposons (TEs) in the P. nodorum genome. I have explored the role of transposon-directed epigenomic suppression in regulating this shift towards virulence. Molecular disruption of the histone methyltransferase (HMT) Dim-5 was found to increase in vitro expression of TE-proximal genes, including the effector Tox1. Similar reactivation of genes in effector-containing repeat islands was achieved through chemical inhibition of 5-mC DNA methylation. These results suggest that co-location with transposons contributes to the in vitro suppression of effector genes by means of epigenomic silencing.
Biography - PhD Student in Peter Slomon lab.