Recombination hotspots inNeurospora crassacontrolled by idiomorphic sequences and meiotic silencing

Abstract

Genes regulating recombination in specific chromosomal intervals ofNeurospora crassawere described in the 1960s but the mechanism is still unknown. For each of therec-1,rec-2andrec-3genes, a single copy of the putative dominant allele, for examplerec-2SLfound in St Lawrence OR74 A wild type, reduces recombination in chromosomal regions specific to that gene. However, when we sequenced the recessive allele,rec-2LG(derived from the Lindegren 1A wild type) we found that a 10 kb region inrec-2SLstrains was replaced by a 2.7 kb unrelated sequence, making the “alleles” idiomorphs. When we introducedsad-1, a mutant lacking the RNA-dependent RNA polymerase that silences unpaired coding regions during meiosis into crosses heterozygousrec-2SL/rec-2LG, it increased recombination, indicating that meiotic silencing of a gene promoting recombination is responsible for dominant suppression of recombination. Consistent with this, mutation ofrec-2LGby RIP (repeat induced mutation) generated an allele with multiple stop codons in the predictedrec-2gene, which does not promote recombination and is recessive torec-2LG.sad-1also relieves suppression of recombination in relevant target regions, in crosses heterozygous forrec-1alleles and in crosses heterozygous forrec-3alleles. We conclude that for all three knownrecgenes, one allele appears dominant only because meiotic silencing prevents the product of the active, “recessive”, allele from stimulating recombination during meiosis. In addition, the proposed amino acid sequence of REC-2 indicates regulation of recombination in Neurospora differs from any currently known mechanism.