The fungus Magnaporthe oryzae is a serious pathogen of rice and other grasses. Telomeric restriction fragments in Magnaporthe isolates that infect perennial ryegrass (prg) are hotspots for genomic rearrangement and undergo frequent, spontaneous alterations during fungal culture. The telomeres of rice-infecting isolates are very stable by comparison. Sequencing of chromosome ends from a number of prg-infecting isolates revealed two related non-LTR retrotransposons (M. oryzae Telomeric Retrotransposons or MoTeRs) inserted in the telomere repeats. This contrasts with rice pathogen telomeres that are uninterrupted by other sequences. Genetic evidence indicates that the MoTeR elements are responsible for the observed instability. MoTeRs represent a new family of telomere-targeted transposons whose members are found exclusively in fungi.T ELOMERES are the sequences that form the ends of linear chromosomes and are essential for maintaining the integrity of terminal DNA. In most organisms, the telomeres are composed of tandem arrays of short sequence motifs that are added on to the 39 ends of chromosomes by telomerase-a specialized reverse transcriptase (Greider and Blackburn 1989;Yu et al. 1990). This prevents the loss of DNA that would normally occur as a result of conservative DNA replication. The telomeres are bound by numerous proteins that shelter the terminal sequences from degradation (Garvik et al. 1995;Vodenicharov and Wellinger 2006) and illegitimate recombination (Dubois et al. 2002). Certain Diptera lack telomerase and, instead, their chromosome termini are maintained by different types of repeats (Saiga and Edstrom 1985;Biessmann et al. 1998;. The most striking example is in Drosophila whose telomeres are composed of arrays of non-LTR retrotransposons George et al. 2006), which are capable of transposing to free DNA ends (Traverse and Pardue 1988;Biessmann et al. 1990). The extension of chromosome ends through the addition of transposon sequences not only solves the end-replication problem but also serves to establish a nucleoprotein complex that is essential for protecting the chromosome ends and maintaining telomere homoeostasis (Fanti et al. 1998;Perrini et al. 2004).In many organisms, the telomeres are attached to a specific sequence that is duplicated (although often not perfectly) at many, and sometimes all, chromosome ends. Such sequences, which usually are TG-rich and often contain short tandem repeats, define a distinct distal subtelomere domain (Pryde et al. 1997). In addition to possessing distally located subtelomere domains, several organisms have proximal domains that contain genes and gene families that are also variously dispersed among different chromosome ends (Pryde et al. 1997). High levels of subtelomere polymorphism are found in many organisms, including vertebrates (Wilkie et al. 1991;Bassham et al. 1998;Baird et al. 2000;Mefford et al. 2001), insects (Biessmann et al. 1998Anderson et al. 2008;Kern and Begun 2008), plants (Yang et al. 2005), and fungi (Naumov et al. 1995Na...

Wheat blast is a devastating disease that was first identified in Brazil and has subsequently spread to surrounding countries in South America. In May 2011, disease scouting in a University of Kentucky wheat trial plot in Princeton, KY identified a single plant with disease symptoms that differed from the Fusarium head blight that was present in surrounding wheat. The plant in question bore a single diseased head that was bleached yellow from a point about one-third up the rachis to the tip. A gray mycelial mass was observed at the boundary of the healthy tissue and microscopic examination of this material revealed pyriform spores consistent with a Magnaporthe sp. The pathogen was subsequently identified as Magnaporthe oryzae through amplification and sequencing of molecular markers, and genome sequencing revealed that the U.S. wheat blast isolate was most closely related to an M. oryzae strain isolated from annual ryegrass in 2002 and quite distantly related to M. oryzae strains causing wheat blast in South America. The suspect isolate was pathogenic to wheat, as indicated by growth chamber inoculation tests. We conclude that this first occurrence of wheat blast in the United States was most likely caused by a strain that evolved from an endemic Lolium-infecting pathogen and not by an exotic introduction from South America. Moreover, we show that M. oryzae strains capable of infecting wheat have existed in the United States for at least 16 years. Finally, evidence is presented that the environmental conditions in Princeton during the spring of 2011 were unusually conducive to the early production of blast inoculum.

The fungus Magnaporthe oryzae causes devastating diseases of crops, including rice and wheat, and in various grasses. Strains from ryegrasses have highly unstable chromosome ends that undergo frequent rearrangements, and this has been associated with the presence of retrotransposons (Magnaporthe oryzae Telomeric Retrotransposons—MoTeRs) inserted in the telomeres. The objective of the present study was to determine the mechanisms by which MoTeRs promote telomere instability. Targeted cloning, mapping, and sequencing of parental and novel telomeric restriction fragments (TRFs), along with MinION sequencing of genomic DNA allowed us to document the precise molecular alterations underlying 109 newly-formed TRFs. These included truncations of subterminal rDNA sequences; acquisition of MoTeR insertions by ‘plain’ telomeres; insertion of the MAGGY retrotransposons into MoTeR arrays; MoTeR-independent expansion and contraction of subtelomeric tandem repeats; and a variety of rearrangements initiated through breaks in interstitial telomere tracts that are generated during MoTeR integration. Overall, we estimate that alterations occurred in approximately sixty percent of chromosomes (one in three telomeres) analyzed. Most importantly, we describe an entirely new mechanism by which transposons can promote genomic alterations at exceptionally high frequencies, and in a manner that can promote genome evolution while minimizing collateral damage to overall chromosome architecture and function.

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