%0 Journal Article
%T Mitochondrial complex I deficiency leads to the retardation of early embryonic development in Ndufs4 knockout mice
%A A-Ni Chi
%A Cong Wan
%A Han Wu
%A Ke Song
%A Mei Wang
%A Xiao-Yang Zhao
%A Ya-Mei Xiao
%A Ya-Ping Huang
%J Archive of "PeerJ".
%D 2017
%R 10.7717/peerj.3339
%X The NDUFS4 gene encodes an 18-kD subunit of mitochondria complex I, and mutations in this gene lead to the development of a severe neurodegenerative disease called Leigh syndrome (LS) in humans. To investigate the disease phenotypes and molecular mechanisms of Leigh syndrome, the Ndufs4 knockout (KO) mouse has been widely used as a novel animal model. Because the homozygotes cannot survive beyond child-bearing age, whether Ndufs4 and mitochondrial complex I influence early embryonic development remains unknown. In our study, we attempted to investigate embryonic development in Ndufs4 KO mice, which can be regarded as a Leigh disease model and were created through the CRISPR (clustered regularly interspaced short palindromic repeat) and Cas9 (CRISPR associated)-mediated genome editing system
%K Mitochondria complex I
%K Ndufs4
%K CRISPR/Cas9
%K Embryo development
%U https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5438584/