Abstract
BackgroundRepeat-induced point mutation (RIP) is a fungal genome defence mechanism guarding against transposon invasion. RIP mutates the sequence of repeated DNA and over time renders the affected regions unrecognisable by similarity search tools such as BLAST.ResultsDeRIP is a new software tool developed to predict the original sequence of a RIP-mutated region prior to the occurrence of RIP. In this study, we apply deRIP to the genome of the wheat pathogen Stagonospora nodorum SN15 and predict the origin of several previously uncharacterised classes of repetitive DNA.ConclusionsFive new classes of transposon repeats and four classes of endogenous gene repeats were identified after deRIP. The deRIP process is a new tool for fungal genomics that facilitates the identification and understanding of the role and origin of fungal repetitive DNA. DeRIP is open-source and is available as part of the RIPCAL suite at http://www.sourceforge.net/projects/ripcal.
Highlights
Repeat-induced point mutation (RIP) is a fungal genome defence mechanism guarding against transposon invasion
Repeat-induced point mutation (RIP) is a genome defence mechanism found within filamentous ascomycete fungi that is purported to combat transposon invasion
In the majority of cases studied so far, there is a strong bias for the mutation of C:G nucleotide base pairs followed by A:T nucleotide base pairs [18,21,22]
Summary
Repeat-induced point mutation (RIP) is a fungal genome defence mechanism guarding against transposon invasion. Putative RIP events have been detected bioinformatically in Aspergillus fumigatus [8], Fusarium oxysporum [9,10,11], Aspergillus nidulans [12], Neurospora tetrasperma [13], Microbotryum violaceum [14], Aspergillus oryzae [15], Magnaporthe oryzae [16], Colletotrichum cereal [17], Aspergillus niger [18], Penicillium chysogenum [18] and most recently in Stagonospora nodorum [19,20] Given this broad distribution, it is reasonable to assume that RIP is widespread across, The mechanism by which RIP operates is yet to be fully understood, but the following observations have been made. In N. crassa, RIP requires ≥ 80% identity of duplicated DNA over a length of ≥ 400 bp [23,24]
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