Department of Molecular Endocrinology, National Research Institute for Child Health and Development, Tokyo, Japan.
Department of Pediatrics, St. Marianna University School of Medicine, Kawasaki, Japan.
Am J Med Genet A. 2019 Sep;179(9):1778-1782. doi: 10.1002/ajmg.a.61275. Epub 2019 Jun 22.
SHOX haploinsufficiency leading to Leri-Weill dyschondrosteosis (LWD) and idiopathic short stature typically results from intragenic mutations or copy-number variations (CNVs) involving SHOX and/or its putative enhancer regions that are distributed in the genomic interval between 400 kb and 840 kb from Xpter/Ypter. Here, we report two sisters with LWD, who carried a deletion in the far-downstream region of SHOX. The 0.62 Mb deletion contained 50 single nucleotide polymorphisms (SNPs) and short insertions and deletions (indels), whose genotypes were linked to SHOX expression levels in the Genotype-Tissue Expression portal. Notably, most of these SNPs/indels accumulated within a ~20 kb interval that was positioned ~900 kb away from Xpter/Ypter. These SNPs/indels showed similar minor allele frequencies, indicating that they reside within a haplotype block. The ~20 kb interval was not evolutionarily conserved; however, it was associated with the previously determined peak of chromosome conformation capture profiling (4C)-seq. Importantly, the deletion in the present cases partially overlapped with CNVs of three previous cases with skeletal deformity and/or short stature. The results indicate that far-downstream CNVs constitute rare genetic causes of SHOX haploinsufficiency. These CNVs possibly impair SHOX expression through copy-number changes of a human-specific cis-regulatory haplotype block. This notion awaits further validation.
SHOX 基因杂合性缺失导致的 Leri-Weill 软骨发育不全症(LWD)和特发性身材矮小症通常是由于 SHOX 及其假定增强子区域的基因内突变或拷贝数变异(CNVs)引起的,这些区域分布在 Xpter/Ypter 之间的基因组间隔 400kb 到 840kb 范围内。在这里,我们报告了两名患有 LWD 的姐妹,她们携带 SHOX 远下游区域的缺失。该 0.62Mb 的缺失包含 50 个单核苷酸多态性(SNP)和短插入/缺失(indel),其基因型与 Genotype-Tissue Expression 门户中的 SHOX 表达水平相关。值得注意的是,这些 SNP/indel 大多数在一个约 20kb 的间隔内积累,该间隔位于 Xpter/Ypter 约 900kb 之外。这些 SNP/indel 具有相似的次要等位基因频率,表明它们位于单倍型块内。该约 20kb 的间隔不具有进化保守性;然而,它与先前确定的染色体构象捕获分析(4C-seq)峰相关。重要的是,本病例中的缺失部分与先前报道的骨骼畸形和/或身材矮小的三个病例的 CNVs 重叠。结果表明,远下游 CNVs 构成 SHOX 基因杂合性缺失的罕见遗传原因。这些 CNVs 可能通过人类特异性顺式调控单倍型块的拷贝数变化来损害 SHOX 表达。这一观点有待进一步验证。