Recombination hotspots in Neurospora crassa controlled by idiomorphic sequences and meiotic silencing.

Genes regulating recombination in specific chromosomal intervals of Neurospora crassa were described in the 1960s but the mechanism is still unknown. For each of the rec-1, rec-2 and rec-3 genes, a single copy of the putative dominant allele, for example rec-2SL found 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 in rec-2SL strains was replaced by a 2.7 kb unrelated sequence, making the "alleles" idiomorphs. When we introduced sad-1, a mutant lacking the RNA-dependent RNA polymerase that silences unpaired coding regions during meiosis into crosses heterozygous rec-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 of rec-2LG by RIP (repeat induced mutation) generated an allele with multiple stop codons in the predicted rec-2 gene, which does not promote recombination and is recessive to rec-2LG. sad-1 also relieves suppression of recombination in relevant target regions, in crosses heterozygous for rec-1 alleles and in crosses heterozygous for rec-3 alleles. We conclude that for all three known rec genes, 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.