The impairment of HCCS leads to MLS syndrome by activating a non-canonical cell death pathway in the brain and eyes

Authors

  • Alessia Indrieri,

  • Ivan Conte,

  • Giancarlo Chesi,

  • Alessia Romano,

  • Jade Quartararo,

  • Rosarita Tatè,

  • Daniele Ghezzi,

  • Massimo Zeviani,

  • Paola Goffrini,

  • Ileana Ferrero,

  • Paola Bovolenta,

  • Brunella Franco

Errata

This article corrects:

  1. The impairment of HCCS leads to MLS syndrome by activating a non-canonical cell death pathway in the brain and eyes Volume 5, Issue 2, 280–293, Article first published online: 22 January 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.

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