Hawkins Nicole A, Kearney Jennifer A
Department of Pharmacology, Northwestern University, Feinberg School of Medicine, Searle 8-520, 320 East Superior St., Chicago, IL 60091, United States; Neuroscience Program, Vanderbilt University, Nashville, TN 37232, United States.
Department of Pharmacology, Northwestern University, Feinberg School of Medicine, Searle 8-520, 320 East Superior St., Chicago, IL 60091, United States; Department of Medicine, Vanderbilt University, Nashville, TN 37232, United States.
Epilepsy Res. 2016 Jan;119:20-3. doi: 10.1016/j.eplepsyres.2015.11.016. Epub 2015 Dec 1.
Mutations in voltage-gated sodium channel genes cause several types of human epilepsies. Often, individuals with the same sodium channel mutation exhibit diverse phenotypes. This suggests that factors beyond the primary mutation influence disease severity, including genetic modifiers. Mouse epilepsy models with voltage-gated sodium channel mutations exhibit strain-dependent phenotype variability, supporting a contribution of genetic modifiers in epilepsy. The Scn2a(Q54) (Q54) mouse model has a strain-dependent epilepsy phenotype. Q54 mice on the C57BL/6J (B6) strain exhibit delayed seizure onset and improved survival compared to [B6xSJL/J]F1.Q54 mice. We previously mapped two dominant modifier loci that influence Q54 seizure susceptibility and identified Hlf (hepatic leukemia factor) as a candidate modifier gene at one locus. Hlf and other PAR bZIP transcription factors had previously been associated with spontaneous seizures in mice thought to be caused by down-regulation of the pyridoxine pathway. An Hlf targeted knockout mouse model was used to evaluate the effect of Hlf deletion on Q54 phenotype severity. Hlf(KO/KO);Q54 double mutant mice exhibited elevated frequency and reduced survival compared to Q54 controls. To determine if direct modulation of the pyridoxine pathway could alter the Q54 phenotype, mice were maintained on a pyridoxine-deficient diet for 6 weeks. Dietary pyridoxine deficiency resulted in elevated seizure frequency and decreased survival in Q54 mice compared to control diet. To determine if Hlf could modify other epilepsies, Hlf(KO/+) mice were crossed with the Scn1a(KO/+) Dravet syndrome mouse model to examine the effect on premature lethality. Hlf(KO/+);Scn1a(KO/+) offspring exhibited decreased survival compared to Scn1a(KO/+) controls. Together these results demonstrate that Hlf is a genetic modifier of epilepsy caused by voltage-gated sodium channel mutations and that modulation of the pyridoxine pathway can also influence phenotype severity.
电压门控钠通道基因突变会引发多种类型的人类癫痫。通常,具有相同钠通道突变的个体表现出多样的表型。这表明除了原发性突变之外的因素会影响疾病严重程度,其中包括遗传修饰因子。具有电压门控钠通道突变的小鼠癫痫模型表现出品系依赖性的表型变异性,这支持了遗传修饰因子在癫痫中的作用。Scn2a(Q54)小鼠模型具有品系依赖性癫痫表型。与[B6xSJL/J]F1.Q54小鼠相比,C57BL/6J(B6)品系的Q54小鼠癫痫发作起始延迟且存活率提高。我们之前定位了两个影响Q54癫痫易感性的显性修饰基因座,并确定Hlf(肝白血病因子)是其中一个基因座上的候选修饰基因。Hlf和其他PAR bZIP转录因子之前被认为与小鼠自发性癫痫有关,推测是由维生素B6途径下调所致。利用一个Hlf靶向敲除小鼠模型来评估Hlf缺失对Q54表型严重程度的影响。与Q54对照相比,Hlf(KO/KO);Q54双突变小鼠癫痫发作频率升高且存活率降低。为了确定直接调节维生素B6途径是否能改变Q54表型,将小鼠维持在缺乏维生素B6的饮食中6周。与对照饮食相比,饮食中缺乏维生素B6导致Q54小鼠癫痫发作频率升高且存活率降低。为了确定Hlf是否能修饰其他癫痫类型,将Hlf(KO/+)小鼠与Scn1a(KO/+)德雷维特综合征小鼠模型杂交,以检查对过早死亡的影响。与Scn1a(KO/+)对照相比,Hlf(KO/+);Scn1a(KO/+)后代存活率降低。这些结果共同表明,Hlf是电压门控钠通道突变所致癫痫的遗传修饰因子,并且维生素B6途径的调节也会影响表型严重程度。