Gladyshev Eugene, Kleckner Nancy
Department of Molecular and Cellular Biology, Harvard University, 52 Oxford Street, Room NW140, Cambridge, MA, 02138, USA.
Curr Genet. 2017 Jun;63(3):389-400. doi: 10.1007/s00294-016-0649-4. Epub 2016 Sep 14.
Numerous cytogenetic observations have shown that homologous chromosomes (or individual chromosomal loci) can engage in specific pairing interactions in the apparent absence of DNA breakage and recombination, suggesting that canonical recombination-mediated mechanisms may not be the only option for sensing DNA/DNA homology. One proposed mechanism for such recombination-independent homology recognition involves direct contacts between intact double-stranded DNA molecules. The strongest in vivo evidence for the existence of such a mechanism is provided by the phenomena of homology-directed DNA modifications in fungi, known as repeat-induced point mutation (RIP, discovered in Neurospora crassa) and methylation-induced premeiotically (MIP, discovered in Ascobolus immersus). In principle, Neurospora RIP can detect the presence of gene-sized DNA duplications irrespectively of their origin, underlying nucleotide sequence, coding capacity or relative, as well as absolute positions in the genome. Once detected, both sequence copies are altered by numerous cytosine-to-thymine (C-to-T) mutations that extend specifically over the duplicated region. We have recently shown that Neurospora RIP does not require MEI-3, the only RecA/Rad51 protein in this organism, consistent with a recombination-independent mechanism. Using an ultra-sensitive assay for RIP mutation, we have defined additional features of this process. We have shown that RIP can detect short islands of homology of only three base-pairs as long as many such islands are arrayed with a periodicity of 11 or 12 base-pairs along a pair of DNA molecules. While the presence of perfect homology is advantageous, it is not required: chromosomal segments with overall sequence identity of only 35-36 % can still be recognized by RIP. Importantly, in order for this process to work efficiently, participating DNA molecules must be able to co-align along their lengths. Based on these findings, we have proposed a model, in which sequence homology is detected by direct interactions between slightly-extended double-stranded DNAs. As a next step, it will be important to determine if the uncovered principles also apply to other processes that involve recombination-independent interactions between homologous chromosomal loci in vivo as well as to protein-free DNA/DNA interactions that were recently observed under biologically relevant conditions in vitro.
大量细胞遗传学观察表明,同源染色体(或单个染色体位点)在明显不存在DNA断裂和重组的情况下能够进行特定的配对相互作用,这表明经典的重组介导机制可能不是感知DNA/DNA同源性的唯一选择。一种针对这种不依赖重组的同源性识别的推测机制涉及完整双链DNA分子之间的直接接触。真菌中同源性指导的DNA修饰现象,即重复诱导点突变(RIP,在粗糙脉孢菌中发现)和减数分裂前甲基化诱导(MIP,在浸没曲霉菌中发现),为这种机制的存在提供了最有力的体内证据。原则上,粗糙脉孢菌的RIP可以检测到基因大小的DNA重复序列的存在,而不管其起源、潜在核苷酸序列、编码能力或在基因组中的相对以及绝对位置如何。一旦检测到,两个序列拷贝都会被大量的胞嘧啶到胸腺嘧啶(C到T)突变所改变,这些突变会特异性地延伸到重复区域。我们最近表明,粗糙脉孢菌的RIP不需要MEI-3,这是该生物体中唯一的RecA/Rad51蛋白,这与不依赖重组的机制一致。使用一种超灵敏的RIP突变检测方法,我们确定了这一过程的其他特征。我们已经表明,只要沿着一对DNA分子有许多这样的三碱基对同源性短岛以11或12碱基对的周期排列,RIP就能检测到只有三个碱基对的同源性短岛。虽然完美同源性的存在是有利的,但并非必需:总体序列同一性仅为35 - 36%的染色体片段仍能被RIP识别。重要的是,为了使这一过程有效地发挥作用,参与的DNA分子必须能够沿其长度共同排列。基于这些发现,我们提出了一个模型,其中序列同源性是通过稍微伸展的双链DNA之间的直接相互作用来检测的。下一步,确定所揭示的原理是否也适用于体内涉及同源染色体位点之间不依赖重组的相互作用的其他过程,以及最近在体外生物学相关条件下观察到的无蛋白质的DNA/DNA相互作用,将是很重要的。