Department of Human & Molecular Genetics, Virginia Commonwealth University, Richmond, Virginia, United States of America.
Department of Pathology, Virginia Commonwealth University, Richmond, Virginia, United States of America.
PLoS One. 2021 Jul 20;16(7):e0254806. doi: 10.1371/journal.pone.0254806. eCollection 2021.
Down syndrome, which results from a trisomic imbalance for chromosome 21, has been associated with 80+ phenotypic traits. However, the cellular changes that arise in somatic cells due to this aneuploid condition are not fully understood. The primary aim of this study was to determine if germline trisomy 21 is associated with an increase in spontaneous somatic cell chromosomal instability frequencies (SCINF). To achieve this aim, we quantified SCINF in people with mosaic Down syndrome using a cytokinesis-blocked micronucleus assay. By comparing values in their isogenic trisomic/disomic cells, we obtained a measure of differences in SCINF that are directly attributable to a trisomy 21 imbalance, since differential effects attributable to "background" genetic factors and environmental exposures could be eliminated. A cross-sectional assessment of 69 people with mosaic Down syndrome (ages 1 to 44; mean age of 12.84 years) showed a significantly higher frequency of micronuclei in their trisomic (0.37 ± 0.35 [mean ± standard deviation]) compared to disomic cells (0.18 ± 0.11)(P <0.0001). The daughter binucleates also showed significantly higher levels of abnormal patterns in the trisomic (1.68 ± 1.21) compared to disomic (0.35 ± 0.45) cells (P <0.0001). Moreover, a significant Age x Cell Type interaction was noted (P = 0.0113), indicating the relationship between age and SCINF differed between the trisomic and disomic cells. Similarly, a longitudinal assessment (mean time interval of 3.9 years; range of 2 to 6 years) of 18 participants showed a mean 1.63-fold increase in SCINF within individuals over time for their trisomic cells (P = 0.0186), compared to a 1.13-fold change in their disomic cells (P = 0.0464). In summary, these results showed a trisomy 21-associated, age-related increase in SCINF. They also underscore the strength of the isogenic mosaic Down syndrome model system for "unmasking" cellular changes arising from a trisomy 21 imbalance.
唐氏综合征是由于 21 号染色体三体不平衡引起的,与 80 多种表型特征有关。然而,由于这种非整倍体条件而在体细胞中出现的细胞变化还没有被完全理解。本研究的主要目的是确定生殖细胞三体 21 是否与自发体细胞染色体不稳定性频率(SCINF)的增加有关。为了实现这一目标,我们使用细胞分裂阻断微核试验来测定镶嵌型唐氏综合征患者的 SCINF。通过比较其同源三体/二倍体细胞中的值,我们获得了直接归因于 21 号染色体三体不平衡的 SCINF 差异的衡量标准,因为可以消除归因于“背景”遗传因素和环境暴露的差异影响。对 69 名镶嵌型唐氏综合征患者(年龄 1 至 44 岁;平均年龄 12.84 岁)进行横断面评估显示,其三体(0.37 ± 0.35[平均值 ± 标准差])中的微核频率明显高于二倍体(0.18 ± 0.11)(P <0.0001)。女儿双核细胞中,三体(1.68 ± 1.21)中的异常模式水平也明显高于二倍体(0.35 ± 0.45)(P <0.0001)。此外,还注意到年龄×细胞类型的显著相互作用(P = 0.0113),表明年龄与 SCINF 之间的关系在三体和二倍体细胞之间有所不同。同样,对 18 名参与者进行的纵向评估(平均时间间隔为 3.9 年;范围为 2 至 6 年)显示,随着时间的推移,个体的三体细胞中的 SCINF 平均增加了 1.63 倍(P = 0.0186),而二倍体细胞中的 SCINF 增加了 1.13 倍(P = 0.0464)。总之,这些结果表明,唐氏综合征 21 号染色体三体相关的、与年龄相关的 SCINF 增加。它们还强调了同源镶嵌型唐氏综合征模型系统在揭示由于 21 号染色体三体不平衡引起的细胞变化方面的优势。