Repeat-modulated population genetic effects in fungal proteins.
A number of fungal lineages, notably N. crassa, have evolved a novel mechanism of processing genomic duplication events known as repeat-induced point (RIP) mutation. This mechanism appears, on the one hand, to act as a conservative genomic safeguard, by introducing stop codons into duplicated nucleotide sequences, thereby preempting consequences such as dosage effects. However, it also typically performs further nonsynonymous (i.e., amino acid-changing) nucleotide substitutions, the significance of which is unclear. We explore here the possibility that RIP-mutated genes which evade silencing may have some microevolutionary impact on functional sequences. Our approach focuses on structurally important hydrophobic/polar (HP) amino-acid substitutions effected by RIP. We exploit a simple generic protein folding model to predict the associated emergence of increased protein-structural stability and variance within a large population.
Braun
F N
FN
Department of Biochemistry and Biophysics, and Stockholm Bioinformatics Center, Stockholm University, 10691, Stockholm, Sweden. chefnb@sbc.su.se
Liberles
D A
DA
D000596:Amino Acids / Q000737:chemistry; D003062:Codon / Q000235:genetics; D005656:Fungal Proteins / Q000235:genetics*; D005658:Fungi / Q000235:genetics*; D020440:Gene Duplication; D020868:Gene Silencing; D005828:Genetics, Population; D008957:Models, Genetic; D008958:Models, Molecular; D017354:Point Mutation / Q000235:genetics*; D017510:Protein Folding
D000596:Amino Acids; D003062:Codon; D005656:Fungal Proteins