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.
Highlights
Pyrenophora teres [anamorph Drechslera teres (Sacc.) Shoemaker] is a haploid ascomycete that causes net blotch in barley
The P. teres f. teres (PTT) isolates used in this study were W1-1 collected from the Wongan Hills, Western Australia (WA) in 2009, Stir 9-2 (South Stirlings, WA, 2009), NB29 (Wongan Hills, WA, 1985), NB73 (Tansey, Queensland, 1994), NB85 (Gatton, Queensland, 1995) and a Canadian isolate, 0-1, collected before 1998 (Weiland et al, 1999)
Older repeat instances subjected to repeat induced point mutation (RIP) G/C-to-A/T transition mutations diverge away from the original canonical form
Summary
Pyrenophora teres [anamorph Drechslera teres (Sacc.) Shoemaker] is a haploid ascomycete that causes net blotch in barley. PTT disease is known as net form net blotch (NFNB) and is characterized by necrotic lesions along leaves with net-like longitudinal and transverse striations. PTM infection results in spot form net blotch (SFNB), which typically shows discrete ovoid lesions (Figure 1). In susceptible cultivars, both diseases spread to encompass entire leaves leading to withering and canopy loss. Artificial hybrids can be readily made in the laboratory (McDonald, 1967; Smedegård-Petersen, 1977a; Campbell and Crous, 2003; Jalli, 2011), PTT and PTM are considered to be genetically autonomous populations (Rau et al, 2003, 2007; Bakonyi and Justesen, 2007; Bogacki et al, 2010; Lehmensiek et al, 2010; Leišová-Svobodová et al, 2014; Akhavan et al, 2016)
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