Cellular and Molecular Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran; Department of Medical Genetics, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Diabetes Research Center, Health Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran; Department of Pediatrics, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Gene. 2025 Jan 30;935:149020. doi: 10.1016/j.gene.2024.149020. Epub 2024 Oct 24.
Biotinidase (BTD, encoded by the BTD gene) deficiency is an autosomal recessive neurometabolic disease caused by abnormal BTD activity in the biotin cycle. The clinical symptoms of patients, which are mainly neurocutaneous, range from mild to severe based on the enzyme activity level. This study aimed to identify BTD gene mutations in suspected BTD deficiency patients for the first time in the southwest of Iran and evaluate their genotype-phenotype correlations.
11 clinically and biochemically suspected patients from nine unrelated families and their available family members were subjected to Sanger sequencing. Segregation analysis was performed for novel mutation. The effect of each mutation on protein stability and hydropathicity, as well as the pathogenicity prediction of all detected mutations were assessed using various in silico analysis tools.
Six mutations including a novel and five previously reported mutations were identified in patients with different ethnicities. Three out of five known mutations were reported for the first time in Iran. Various common clinical manifestations and a rarely reported coexistence of celiac disease in biotinidase deficiency patients were observed. The novel missense variant c.787G > A (p.Glu263Lys) was detected in exon 4 of the BTD gene, within the biotinidase-like domain of the BTD protein. This variation was found in two cousins of a family, both developed the same initial clinical presentation. In silico analyses revealed that this missense substitution decreased protein stability and increased protein hydrophilicity. Additionally, the known frameshift mutation c.1264delG (p.val422serfster59), was the most frequent allele in the studied population. We also predicted and visualized the effects of the novel and frameshift mutations on protein structure.
Our findings expanded the mutational spectrum of the BTD gene and provided valuable data on genotype-phenotype correlations, which helps in genetic counseling. Furthermore, the necessity of performing molecular analysis along with enzymatic analysis was highlighted by this study.
生物素酶(BTD,由 BTD 基因编码)缺乏症是一种常染色体隐性神经代谢疾病,由生物素循环中 BTD 活性异常引起。患者的临床症状主要为神经皮肤,根据酶活性水平,从轻度到重度不等。本研究旨在首次在伊朗西南部鉴定疑似 BTD 缺乏症患者的 BTD 基因突变,并评估其基因型-表型相关性。
对来自 9 个无关家庭的 11 例临床和生化疑似患者及其可利用的家庭成员进行 Sanger 测序。对新突变进行分离分析。使用各种计算分析工具评估每个突变对蛋白质稳定性和疏水性的影响,以及所有检测到的突变的致病性预测。
在不同种族的患者中鉴定出 6 种突变,包括一种新突变和 5 种以前报道的突变。以前在伊朗报道的 5 种已知突变中的 3 种首次报道。观察到生物素酶缺乏症患者存在各种常见的临床表现和罕见的乳糜泻共存。在 BTD 基因的外显子 4 中检测到新型错义变异 c.787G>A(p.Glu263Lys),位于 BTD 蛋白的生物素酶样结构域内。这种变异在一个家庭的两个表亲中发现,他们都出现了相同的初始临床表现。计算分析表明,这种错义取代降低了蛋白质稳定性并增加了蛋白质的亲水性。此外,研究人群中最常见的等位基因为已知的移码突变 c.1264delG(p.val422serfster59)。我们还预测并可视化了新型和移码突变对蛋白质结构的影响。
我们的研究结果扩展了 BTD 基因突变谱,并提供了关于基因型-表型相关性的有价值数据,有助于遗传咨询。此外,本研究强调了在进行分子分析的同时进行酶分析的必要性。