Musio Antonio, Mariani Tullio, Montagna Cristina, Zambroni Desirèe, Ascoli Cesare, Ried Thomas, Vezzoni Paolo
Istituto di Tecnologie Biomediche, Dipartimento Genoma Umano, C.N.R., Via Fratelli Cervi, 93, I-20090 Segrate, Mi, Italy.
Gene. 2004 Apr 28;331:33-40. doi: 10.1016/j.gene.2004.01.028.
Roberts syndrome is an autosomal recessive disorder characterised primarily by symmetric reduction of all limbs and growth retardation. Patients have been reported to have premature separation of heterochromatin regions of many chromosomes and abnormalities in cell cycle. Given the rarity of the syndrome, the linkage analysis approach is not suitable to identify the responsible gene. In this work, a cell line derived from a patient affected by Roberts syndrome was characterized by cell biology and molecular cytogenetics, including comparative genomic hybridization and spectral karyotype. No recurrent chromosomal rearrangements were identified. Thereafter, based on the fact that premature chromatide separation is a reliable marker of the disease, we used antisense oligonucleotide technologies to inhibit six genes involved in various steps of the correct chromosome segregation, such as chromosome cohesion, kinetochore assembling, spindle checkpoint and spindle formation. We found that the inhibition of INCENP, ZWINT-1, ZW10 genes results in the appearance of mitotic cells characterised by centromere separation, chromosome aneuploidy and micronuclei formation. In addition, INCENP, ZWINT-1, ZW10 antisense-treated chromosome morphology was very similar to that of Roberts chromosome when analysed by atomic force microscopy. We concluded that INCENP, ZWINT-1, ZW10 gene inhibition results in cellular phenocopies of Roberts syndrome. Taken together, these findings support a possible role of these genes in the pathogenesis of Roberts syndrome.
罗伯茨综合征是一种常染色体隐性疾病,主要特征为所有肢体的对称性发育不全和生长迟缓。据报道,患者存在许多染色体异染色质区域的过早分离以及细胞周期异常。鉴于该综合征的罕见性,连锁分析方法不适用于鉴定致病基因。在这项研究中,我们对源自一名罗伯茨综合征患者的细胞系进行了细胞生物学和分子细胞遗传学特征分析,包括比较基因组杂交和光谱核型分析。未发现复发性染色体重排。此后,基于染色单体过早分离是该疾病的可靠标志物这一事实,我们使用反义寡核苷酸技术抑制了六个参与正确染色体分离各个步骤的基因,如染色体黏连、动粒组装、纺锤体检查点和纺锤体形成。我们发现,抑制INCENP、ZWINT - 1、ZW10基因会导致有丝分裂细胞出现着丝粒分离、染色体非整倍性和微核形成的特征。此外,通过原子力显微镜分析,经INCENP、ZWINT - 1、ZW10反义处理后的染色体形态与罗伯茨综合征染色体非常相似。我们得出结论,抑制INCENP、ZWINT - 1、ZW10基因会导致罗伯茨综合征的细胞表型模拟。综上所述,这些发现支持了这些基因在罗伯茨综合征发病机制中可能发挥的作用。