Location: Cereal Crops ResearchTitle: Transposable element genomic fissuring in Pyrenophora teres is associated with genome expansion and dynamics of host-pathogen genetic interactions
|SYME, ROBERT - Curtin University
|MARTIN, ANKE - University Of Southern Queensland
|WYATT, NATHAN - North Dakota State University
|LAWRENCE, JULIE - Diversity Arrays Technology
|MURIA-GONZALEZ, MARIANO - Curtin University
|ELLWOOD, SIMON - Curtin University
Submitted to: Frontiers in Genetics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/3/2018
Publication Date: 4/18/2018
Citation: Syme, R.A., Martin, A., Wyatt, N.A., Lawrence, J.A., Muria-Gonzalez, M.J., Friesen, T.L., Ellwood, S.R. 2018. Transposable element genomic fissuring in Pyrenophora teres is associated with genome expansion and dynamics of host-pathogen genetic interactions. Frontiers in Genetics. 9:130. https://doi.org/10.3389/fgene.2018.00130.
Interpretive Summary: Net blotch of barley is the most destructive foliar disease of barley in the United States and in many other parts of the world where barley is grown. This disease is caused by two forms of the same fungal species Pyrenophora teres f. teres (PTT) which causes net form net blotch and P. teres f. maculata (PTM) which causes spot form net blotch. The spot form has more recently emerged, however, both forms cause significant yield loss in barley. Some work has been done to characterize the host resistance to both of these forms with more work being done on the net form than the spot form. However, very little has been done to understand the genomic differences between these two forms from the fungal perspective. Understanding of the pathogen is critical to solving this major economic problem in barley production. High quality nearly complete genome sequences were assembled for both forms. The genomes of PTT and PTM are each composed of 12 highly similar chromosomes, however PTT is larger due to expansion from repetitive elements. PTT appears to have a longer cultivated host association than PTM. Gene differences between the forms of P. teres are mainly associated with gene-sparse regions, with many of these genes possessing characteristics of fungal effectors, genes that are known to be involved in virulence. This study provides genomic resources for functional genetics to help dissect factors underlying the host–pathogen interactions.
Technical Abstract: Pyrenophora teres, P. teres f. teres (PTT) and P. teres f. maculata (PTM) cause significant diseases in barley, but little is known about the large-scale genomic differences that may distinguish the two forms. Comprehensive genome assemblies were constructed from long DNA reads, optical and genetic maps. As repeat masking in fungal genomes influences the final gene annotations, an accurate and reproducible pipeline was developed to ensure comparability between isolates. The genomes of the two forms are highly collinear, each composed of 12 chromosomes. Genome evolution in P. teres is characterized by genome fissuring through the insertion and expansion of transposable elements (TEs), a process that isolates blocks of genic sequence. The phenomenon is particularly pronounced in PTT, which has a larger, more repetitive genome than PTM and more recent transposon activity measured by the frequency and size of genome fissures. PTT has a longer cultivated host association and, notably, a greater range of host–pathogen genetic interactions compared to other Pyrenophora spp., a property which associates better with genome size than pathogen lifestyle. The two forms possess similar complements of TE families with Tc1/Mariner and LINE-like Tad-1 elements more abundant in PTT. Tad-1 was only detectable as vestigial fragments in PTM and, within the forms, differences in genome sizes and the presence and absence of several TE families indicated recent lineage invasions. Gene differences between P. teres forms are mainly associated with gene-sparse regions near or within TE-rich regions, with many genes possessing characteristics of fungal effectors. Instances of gene interruption by transposons resulting in pseudogenization were detected in PTT. In addition, both forms have a large complement of secondary metabolite gene clusters indicating significant capacity to produce an array of different molecules. This study provides genomic resources for functional genetics to help dissect factors underlying the host–pathogen interactions.