Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA.
Nat Genet. 2011 Oct 2;43(11):1074-81. doi: 10.1038/ng.944.
We identified complex genomic rearrangements consisting of intermixed duplications and triplications of genomic segments at the MECP2 and PLP1 loci. These complex rearrangements were characterized by a triplicated segment embedded within a duplication in 11 unrelated subjects. Notably, only two breakpoint junctions were generated during each rearrangement formation. All the complex rearrangement products share a common genomic organization, duplication-inverted triplication-duplication (DUP-TRP/INV-DUP), in which the triplicated segment is inverted and located between directly oriented duplicated genomic segments. We provide evidence that the DUP-TRP/INV-DUP structures are mediated by inverted repeats that can be separated by >300 kb, a genomic architecture that apparently leads to susceptibility to such complex rearrangements. A similar inverted repeat-mediated mechanism may underlie structural variation in many other regions of the human genome. We propose a mechanism that involves both homology-driven events, via inverted repeats, and microhomologous or nonhomologous events.
我们鉴定出 MECP2 和 PLP1 基因座的基因组片段混合重复和三倍性的复杂基因组重排。这些复杂重排在 11 个无关个体中表现为嵌合的三重复段位于重复内。值得注意的是,每次重排形成过程中仅产生两个断裂点连接。所有复杂重排产物均具有共同的基因组组织,重复-反转三倍性-重复(DUP-TRP/INV-DUP),其中三重复段反转并位于直接定向重复基因组片段之间。我们提供的证据表明,DUP-TRP/INV-DUP 结构是由可分离超过 300kb 的反向重复介导的,这种基因组结构显然导致了对这种复杂重排的易感性。类似的反向重复介导的机制可能是人类基因组中许多其他区域结构变异的基础。我们提出了一种涉及同源驱动事件(通过反向重复)以及微同源或非同源事件的机制。