Homology-dependent inactivation of LTR retrotransposons in Aspergillus fumigatus and A. nidulans genomes

• Published in: Molecular biology (New York) Vol. 41; no. 6; pp. 886 - 893
• Main Authors: Novikova, O S, Fet, V, Blinov, A G
• Format: Journal Article
• Language: English
• Published: New York Springer Nature B.V 01.12.2007
• Subjects: Ascomycetes; Aspergillus fumigatus; Aspergillus nidulans; CpG islands; Enzymes; Gene silencing; Genetics; Genomes; Mutagenesis; Mutation; Neurospora crassa; Point mutation; Repeated DNA sequences; Retrotransposons
• ISSN: 0026-8933; 1608-3245
• DOI: 10.1134/S0026893307060039

The repeat-induced point mutation mechanism (RIP) is the most intriguing among the known mechanisms of homology-dependent gene inactivation (silencing) because of its ability to produce irreversible mutations in repetitive DNA sequences. Discovered for the first time in Neurospora crassa, RIP is characterized by C:G to T:A transitions in duplicated sequences. The mechanisms and range of occurrence of RIP are still poorly understood. Mobile elements, including retrotransposons, are a common target for the processes that lead to homology-dependent silencing because of their ability to propagate themselves. Comparative analysis of LTR retrotransposons was performed throughout the genomes of two ascomycetes, Aspergillus fumigatus and A. nidulans. "De-RIP" retroelements were reconstructed on the basis of several copies. CpG, CpA, and TpG sites, which are potential targets for mutagenesis, were found at a much lower frequency in mobile elements than in structural genes. The dinucleotide targets of the two species are affected by RIP at different frequencies: mutagenesis occurs at both CpG and CpA sites in A. fumigatus and is confined to CpG dinucleotides in A. nidulans. This work provides a theoretical background for planning the experimental investigation of RIP inactivation in aspergilli.[PUBLICATION ABSTRACT]