Loss of the scavenger mRNA decapping enzyme DCPS causes syndromic intellectual disability with neuromuscular defects.

Article Details

Citation

Ng CK, Shboul M, Taverniti V, Bonnard C, Lee H, Eskin A, Nelson SF, Al-Raqad M, Altawalbeh S, Seraphin B, Reversade B

Loss of the scavenger mRNA decapping enzyme DCPS causes syndromic intellectual disability with neuromuscular defects.

Hum Mol Genet. 2015 Jun 1;24(11):3163-71. doi: 10.1093/hmg/ddv067. Epub 2015 Feb 24.

PubMed ID
25712129 [ View in PubMed
]
Abstract

mRNA decay is an essential and active process that allows cells to continuously adapt gene expression to internal and environmental cues. There are two mRNA degradation pathways: 3' to 5' and 5' to 3'. The DCPS protein is the scavenger mRNA decapping enzyme which functions in the last step of the 3' end mRNA decay pathway. We have identified a DCPS pathogenic mutation in a large family with three affected individuals presenting with a novel recessive syndrome consisting of craniofacial anomalies, intellectual disability and neuromuscular defects. Using patient's primary cells, we show that this homozygous splice mutation results in a DCPS loss-of-function allele. Diagnostic biochemical analyses using various m7G cap derivatives as substrates reveal no DCPS enzymatic activity in patient's cells. Our results implicate DCPS and more generally RNA catabolism, as a critical cellular process for neurological development, normal cognition and organismal homeostasis in humans.

DrugBank Data that Cites this Article

Polypeptides
NameUniProt ID
m7GpppX diphosphataseQ96C86Details