How homologous DNA duplexes in chromosomes are checked for correct alignment prior to exchange of genetic information during meiosis in Eukaryotes is a longstanding puzzle (1), a gap in our knowledge of the molecular processes essential for evolution in the more complex cellular organisms that include fungi, plants, and primates. A mechanism to check correct alignment of homologous DNA duplexes prior to committing to irreversible recombination is essential to limit the usually disastrous consequences of scrambling DNA sequences at random. Early sets of hypotheses for this check involved strand breaks in one duplex and transfer of a strand by RecA proteins to form Watson–Crick base pairing in an intact homologous duplex. These models were attractive as when strand invasion found a homologous sequence, a precursor of a complete exchange event was established. A degree of imperfection in base pairing could lead to a reversal of strand invasion and repair of the initiating duplex. Discovery that recombination is initiated by two strand breaks (2), rather than more reliably repaired single-strand nicks, complicates but does not eliminate such models. Alternatively, appropriate contortions of DNA that might lead to homology detection between intact DNA duplexes have also been considered (3).

中文翻译：

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模型和建模者提供了对同源 DNA 双链体配对的深入了解 [遗传学]

如何在真核生物减数分裂期间交换遗传信息之前检查染色体中的同源 DNA 双链是否正确排列是一个长期存在的难题（1)，我们对更复杂的细胞生物（包括真菌、植物和灵长类动物）进化所必需的分子过程的知识存在差距。在进行不可逆重组之前检查同源 DNA 双链体的正确比对的机制对于限制随机扰乱 DNA 序列的通常灾难性后果至关重要。该检查的早期假设包括一个双链体中的链断裂和 RecA 蛋白转移一条链以在完整的同源双链体中形成 Watson-Crick 碱基配对。这些模型很有吸引力，因为当链入侵发现同源序列时，就建立了完全交换事件的前兆。碱基配对的一定程度的缺陷可能导致链入侵和起始双链体修复的逆转。2 )，而不是更可靠地修复单链缺口，使此类模型复杂化但不会消除。或者，还考虑了可能导致完整 DNA 双链体之间同源性检测的适当 DNA 扭曲 ( 3 )。