Guerrero-Castillo Sergio, Grün Alice, Lewandowski Nicole, Gundorova Polina, Blettenberger Lisa Ela, Laubach Nora Constanze, Küchler Katrin, Barroso Madalena, Uetrecht Charlotte, Gersting Søren W
University Children's Research@Kinder-UKE, University Medical Center Hamburg-Eppendorf (UKE), 20246, Hamburg, Germany.
German Center for Child and Adolescent Health (DZKJ), Partner Site Hamburg, University Medical Center Hamburg-Eppendorf (UKE), 20246, Hamburg, Germany.
Sci Rep. 2025 Oct 23;15(1):37168. doi: 10.1038/s41598-025-24684-3.
Medium-chain specific acyl-CoA dehydrogenase (MCAD) is a mitochondrial homotetrameric flavoprotein that catalyzes the first step in fatty acid beta-oxidation. MCAD deficiency arises from variants that either impair enzymatic activity or destabilize interactions between subunits, leading to protein aggregation. Standard enzymatic assays measure the overall MCAD activity but cannot differentiate between tetramers and other protein forms-critical for understanding the impact of pathogenic variants on structure destabilization. In this study, we adapted a native gel colorimetric assay to quantify the activity of MCAD tetramers separately from other protein forms, providing novel insights into how pathogenic variants affect MCAD structure and function. The assay showed a linear correlation between protein amount and enzymatic activity for octanoyl-CoA, a physiological MCAD substrate. Applying this method to clinically relevant MCAD variants allowed us to distinguish subtle differences in protein shape, enzymatic activity, and FAD content, offering profound implications for understanding the molecular basis of MCADD. This methodology can be extended to analyze variants in other acyl-CoA dehydrogenase family members-such as glutaryl-CoA, isovaleryl-CoA or short-chain fatty acyl-CoA dehydrogenases-that are implicated in disorders of fatty acid and amino acid metabolism.
中链特异性酰基辅酶A脱氢酶(MCAD)是一种线粒体同四聚体黄素蛋白,催化脂肪酸β-氧化的第一步。MCAD缺乏症源于损害酶活性或破坏亚基间相互作用的变体,导致蛋白质聚集。标准酶促测定法测量的是总体MCAD活性,但无法区分四聚体和其他蛋白质形式,而这对于理解致病变体对结构不稳定的影响至关重要。在本研究中,我们采用了一种天然凝胶比色测定法,以将MCAD四聚体的活性与其他蛋白质形式分开进行量化,从而为致病变体如何影响MCAD结构和功能提供了新的见解。该测定法显示,对于生理MCAD底物辛酰辅酶A,蛋白量与酶活性之间呈线性相关。将此方法应用于临床相关的MCAD变体,使我们能够区分蛋白质形状、酶活性和FAD含量的细微差异,这对于理解MCADD的分子基础具有深远意义。这种方法可扩展用于分析其他酰基辅酶A脱氢酶家族成员中的变体,如戊二酰辅酶A、异戊酰辅酶A或短链脂肪酰辅酶A脱氢酶,这些酶与脂肪酸和氨基酸代谢紊乱有关。