Max Planck Institute of Psychiatry, Munich, Germany.
PLoS One. 2013 Jul 16;8(7):e68645. doi: 10.1371/journal.pone.0068645. Print 2013.
SLC6A15 is a neuron-specific neutral amino acid transporter that belongs to the solute carrier 6 gene family. This gene family is responsible for presynaptic re-uptake of the majority of neurotransmitters. Convergent data from human studies, animal models and pharmacological investigations suggest a possible role of SLC6A15 in major depressive disorder. In this work, we explored potential functional variants in this gene that could influence the activity of the amino acid transporter and thus downstream neuronal function and possibly the risk for stress-related psychiatric disorders. DNA from 400 depressed patients and 400 controls was screened for genetic variants using a pooled targeted re-sequencing approach. Results were verified by individual re-genotyping and validated non-synonymous coding variants were tested in an independent sample (N = 1934). Nine variants altering the amino acid sequence were then assessed for their functional effects by measuring SLC6A15 transporter activity in a cellular uptake assay. In total, we identified 405 genetic variants, including twelve non-synonymous variants. While none of the non-synonymous coding variants showed significant differences in case-control associations, two rare non-synonymous variants were associated with a significantly increased maximal (3)H proline uptake as compared to the wildtype sequence. Our data suggest that genetic variants in the SLC6A15 locus change the activity of the amino acid transporter and might thus influence its neuronal function and the risk for stress-related psychiatric disorders. As statistically significant association for rare variants might only be achieved in extremely large samples (N >70,000) functional exploration may shed light on putatively disease-relevant variants.
SLC6A15 是一种神经元特异性中性氨基酸转运体,属于溶质载体 6 基因家族。该基因家族负责大多数神经递质的突触前再摄取。来自人类研究、动物模型和药理学研究的收敛数据表明,SLC6A15 可能在重度抑郁症中起作用。在这项工作中,我们探索了该基因中可能影响氨基酸转运体活性的潜在功能变体,从而影响下游神经元功能,并可能影响与应激相关的精神障碍的风险。使用 pooled targeted re-sequencing 方法对 400 名抑郁症患者和 400 名对照者的 DNA 进行了遗传变异筛选。结果通过个体重测序进行验证,在独立样本中测试了验证的非同义编码变异(N = 1934)。然后,通过测量细胞摄取测定中的 SLC6A15 转运体活性,评估了改变氨基酸序列的九个变体的功能效应。总共鉴定了 405 个遗传变异,包括 12 个非同义变异。虽然在病例对照关联中没有发现任何非同义编码变异具有显著差异,但两种罕见的非同义变异与与野生型序列相比,显著增加了 3H 脯氨酸的最大摄取。我们的数据表明,SLC6A15 基因座中的遗传变异改变了氨基酸转运体的活性,从而可能影响其神经元功能和与应激相关的精神障碍的风险。由于罕见变异的统计学显著关联可能仅在极大数据样本(N > 70,000)中实现,因此功能探索可能会揭示潜在与疾病相关的变异。