PUBLICATION

A Missense Variant in PDK1 Associated with Severe Neurodevelopmental Delay and Epilepsy

Authors
Vaz, R., Wincent, J., Elfissi, N., Rosengren Forsblad, K., Pettersson, M., Naess, K., Wedell, A., Wredenberg, A., Lindstrand, A., Ygberg, S.
ID
ZDB-PUB-221224-6
Date
2022
Source
Biomedicines   10(12): (Journal)
Registered Authors
Keywords
epilepsy, neurodevelopmental delay, pyruvate dehydrogenase kinase, zebrafish
MeSH Terms
none
PubMed
36551928 Full text @ Biomedicines
Abstract
The pyruvate dehydrogenase complex (PDC) is responsible for the conversion of pyruvate into acetyl-CoA, which is used for energy conversion in cells. PDC activity is regulated by phosphorylation via kinases and phosphatases (PDK/PDP). Variants in all subunits of the PDC and in PDK3 have been reported, with varying phenotypes including lactic acidosis, neurodevelopmental delay, peripheral neuropathy, or seizures. Here, we report a de novo heterozygous missense variant in PDK1 (c.1139G > A; p.G380D) in a girl with developmental delay and early onset severe epilepsy. To investigate the role of PDK1G380D in energy metabolism and neuronal development, we used a zebrafish model. In zebrafish embryos we show a reduced number of cells with mitochondria with membrane potential, reduced movements, and a delay in neuronal development. Furthermore, we observe a reduction in the phosphorylation of PDH-E1α by PDKG380D, which suggests a disruption in the regulation of PDC activity. Finally, in patient fibroblasts, a mild reduction in the ratio of phosphorylated PDH over total PDH-E1α was detected. In summary, our findings support the notion that this aberrant PDK1 activity is the cause of clinical symptoms in the patient.
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