The impairment of HCCS leads to MLS syndrome by activating a non-canonical cell death pathway in the brain and eyes
Article first published online: 3 JUN 2014
© 2014 The Authors. Published under the terms of the CC BY license
This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
EMBO Molecular Medicine
Volume 6, Issue 6, page 849, June 2014
How to Cite
Correction to: EMBO Mol Med (2013) 5: 280–293. DOI 10.1002/emmm.201201739
- Issue published online: 3 JUN 2014
- Article first published online: 3 JUN 2014
Vol. 5, Issue 2, 280–293, Article first published online: 22 JAN 2013
In the above article, holo-cytochrome c-type synthase was used instead of holocytochrome c-type synthase, the official gene name. This error occurs in three places in the text and the correct sentences should read:
In the abstract:
Now we provide the evidence that non-canonical mitochondrial-dependent apoptosis explains the phenotype of microphthalmia with linear skin lesions (MLS), an X-linked developmental disorder caused by mutations in the holocytochrome c-type synthase (HCCS) gene.
In the introduction:
HCCS is a highly conserved gene from fungi to metazoans and encodes a mitochondrial holocytochrome c (Cytc)-type synthase, also known as ‘heme lyase’, located on the outer surface of the inner mitochondrial membrane (Schaefer et al, 1996; Schwarz & Cox, 2002).
In ‘The paper explained’ section:
We demonstrate that inactivation of holocytochrome c-type synthase (HCCS), a transcript important for the mitochondrial respiratory chain (MRC), is associated with unconventional activation of caspase-9 in the mitochondria triggered by MRC impairment and overproduction of reactive oxygen species.