Centre intersectoriel en santé durable, Université du Québec à Chicoutimi, Saguenay, QC, Canada.
Département des Sciences Fondamentales, Université du Québec à Chicoutimi, Saguenay, QC, Canada.
Mol Genet Genomic Med. 2020 Jan;8(1):e992. doi: 10.1002/mgg3.992. Epub 2019 Oct 2.
This study reports the genetic features of four Caucasian males from the Saguenay-Lac-St-Jean region affected by partial agenesis of the corpus callosum (ACC) with hypotonia, epilepsy, developmental delay, microcephaly, hypoplasia, and autistic behavior.
We performed whole exome sequencing (WES) to identify new genes involved in this pathological phenotype. The regions of interest were subsequently sequenced for family members.
Single-nucleotide variations (SNVs) and insertions or deletions were detected in genes potentially implicated in brain defects observed in these patients. One patient did not have mutations in genes related to ACC, but carried a de novo pathogenic mutation in Mucolipin-1 (MCOLN1) and was diagnosed with mucolipidosis type IV. Among the other probands, missense SNVs were observed in DCLK2 (Doublecortin Like Kinase 2), HERC2 (HECT And RLD Domain Containing E3 Ubiquitin Protein Ligase 2), and KCNH3 (Potassium channel, voltage-gated, subfamily H, member 3). One patient also carried a non-frameshift insertion in CACNA1A (Cav2.1(P/Q-type) calcium channels).
Although no common genetic defect was observed in this study, we provide evidence for new avenues of investigation for ACC, such as molecular pathways involving HERC2, CACNA1A, KCNH3, and more importantly DCLK2. We also allowed to diagnose an individual with mucolipidosis type IV.
本研究报告了来自萨格奈-圣让地区的 4 名白种男性的遗传特征,他们患有部分胼胝体发育不全(ACC)伴张力减退、癫痫、发育迟缓、小头畸形、发育不良和自闭症行为。
我们进行了全外显子组测序(WES),以鉴定与这些患者脑缺陷相关的新基因。随后对有兴趣的区域进行了家系成员的测序。
在可能与 ACC 相关的基因中检测到单核苷酸变异(SNVs)和插入或缺失。一名患者在与 ACC 相关的基因中没有突变,但携带 Mucolipin-1(MCOLN1)的新生致病性突变,并被诊断为 mucolipidosis 型 IV。在其他先证者中,观察到 Doublecortin Like Kinase 2(DCLK2)、HECT And RLD Domain Containing E3 Ubiquitin Protein Ligase 2(HERC2)和 Potassium channel, voltage-gated, subfamily H, member 3(KCNH3)中的错义 SNVs。一名患者还携带 CACNA1A(Cav2.1(P/Q-type) 钙通道)中的非移码插入。
尽管本研究未观察到共同的遗传缺陷,但我们为 ACC 的新研究途径提供了证据,例如涉及 HERC2、CACNA1A、KCNH3 等的分子途径,更重要的是 DCLK2。我们还能够诊断出一例 mucolipidosis 型 IV。