Toyota Tomoko, Yoshitsugu Kiyoshi, Ebihara Mitsuru, Yamada Kazuo, Ohba Hisako, Fukasawa Masayuki, Minabe Yoshio, Nakamura Kazuhiko, Sekine Yoshimoto, Takei Noriyoshi, Suzuki Katsuaki, Itokawa Masanari, Meerabux Joanne M A, Iwayama-Shigeno Yoshimi, Tomaru Yoshiro, Shimizu Hiromitsu, Hattori Eiji, Mori Norio, Yoshikawa Takeo
Laboratory for Molecular Psychiatry, RIKEN Brain Science Institute, Wako, Saitama, Japan.
Hum Mol Genet. 2004 Mar 1;13(5):551-61. doi: 10.1093/hmg/ddh047. Epub 2004 Jan 6.
The increased incidence of minor physical anomalies (MPAs) in schizophrenia is the fundamental basis for the neurodevelopmental hypothesis of schizophrenia etiology. Ocular misalignment, or strabismus, falls into the category of MPAs, but this phenotype has not been assessed in schizophrenia. This study reveals that a subtype of strabismus, constant exotropia, displays marked association with schizophrenia (P=0.00000000906). To assess the genetic mechanisms, we examined the transcription factor genes ARIX (recently identified as a causative gene for syndromic strabismus) and its paralogue, PMX2B. We identified frequent deletion/insertion polymorphisms in the 20-alanine homopolymer stretch of PMX2B, with a modest association between these functional polymorphisms and constant exotropia in schizophrenia (P=0.029). The polymorphisms were also associated with overall schizophrenia (P=0.012) and more specifically with schizophrenia manifesting strabismus (P=0.004). These results suggest a possible interaction between PMX2B and other schizophrenia-precipitating factors, increasing the risk of the combined phenotypes. This study also highlights the unique nature of the polyalanine length variations found in PMX2B. In contrast with other transcription factor genes, the variations in PMX2B show a high prevalence, with deletions being more common than insertions. Additionally, the polymorphisms are of ancient origin and stably transmitted, with mild phenotypic effects. In summary, our study lends further support to the disruption of neurodevelopment in the etiology of schizophrenia, by demonstrating the association of a specific MPA, in this case, constant exotropia with schizophrenia, along with molecular variations in a possible causative gene.
精神分裂症中轻微身体异常(MPA)发病率的增加是精神分裂症病因神经发育假说的根本基础。眼球斜视,即斜视,属于MPA的范畴,但尚未在精神分裂症中对这种表型进行评估。本研究表明,斜视的一种亚型,恒定性外斜视,与精神分裂症有显著关联(P = 0.00000000906)。为了评估遗传机制,我们研究了转录因子基因ARIX(最近被确定为综合征性斜视的致病基因)及其旁系同源基因PMX2B。我们在PMX2B的20个丙氨酸同聚物延伸区域发现了频繁的缺失/插入多态性,这些功能多态性与精神分裂症中的恒定性外斜视之间存在适度关联(P = 0.029)。这些多态性也与总体精神分裂症相关(P = 0.012),更具体地说,与表现为斜视的精神分裂症相关(P = 0.004)。这些结果表明PMX2B与其他精神分裂症诱发因素之间可能存在相互作用,增加了合并表型的风险。本研究还突出了PMX2B中发现的多聚丙氨酸长度变异的独特性质。与其他转录因子基因相比,PMX2B中的变异具有较高的发生率,缺失比插入更常见。此外,这些多态性起源古老且稳定遗传,具有轻微的表型效应。总之,我们的研究通过证明一种特定的MPA(在本病例中为恒定性外斜视)与精神分裂症的关联以及可能的致病基因中的分子变异,进一步支持了精神分裂症病因中神经发育的破坏。