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 Point 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 suggests that regulation of recombination in Neurospora differs from any currently known mechanism.

中文翻译：

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粗糙脉孢菌中的重组热点受独特型序列和减数分裂沉默控制。

粗糙脉孢菌特定染色体间隔内调节重组的基因在 20 世纪 60 年代已被描述，但其机制仍不清楚。对于每个rec-1、rec-2和rec-3基因，推定的显性等位基因的单个拷贝，例如在圣劳伦斯OR74A野生型中发现的rec-2SL，减少了该基因特异的染色体区域中的重组。然而，当我们对隐性等位基因rec-2LG（源自Lindegren 1A野生型）进行测序时，我们发现rec-2SL菌株中的10 kb区域被2.7 kb无关序列取代，从而形成“等位基因”特性。当我们将sad-1（一种缺乏RNA依赖性RNA聚合酶的突变体，在减数分裂过程中沉默未配对的编码区）引入杂合rec-2SL/rec-2LG时，它增加了重组，表明促进重组的基因的减数分裂沉默负责重组的显性抑制。与此一致，RIP（重复诱导点突变）对rec-2LG的突变在预测的rec-2基因中产生了具有多个终止密码子的等位基因，该等位基因不促进重组并且对rec-2LG是隐性的。Sad-1 还可以缓解相关靶区域、rec-1 等位基因杂合杂交和 rec-3 等位基因杂合杂交中重组的抑制。我们得出的结论是，对于所有三个已知的rec基因，一个等位基因之所以表现出显性，只是因为减数分裂沉默阻止了活性“隐性”等位基因的产物在减数分裂期间刺激重组。此外，所提出的 REC-2 氨基酸序列表明脉孢菌中的重组调节不同于任何目前已知的机制。