Deleted in cancer 1 (DICE1) is an essential protein controlling the topology of the inner mitochondrial membrane in C. elegans

Sung Min Han, Tae Hoon Lee, Ji Young Mun, Moon Jeong Kim, Ekaterini A. Kritikou, Se Jin Lee, Sung Sik Han, Michael O. Hengartner, Hyeon Sook Koo

Research output: Contribution to journalArticlepeer-review

20 Citations (Scopus)


DICE1 (deleted in cancer 1), first identified in human lung carcinoma cell lines, is a candidate tumor suppressor, but the details of its activity remain largely unknown. We have found that RNA interference of its C. elegans homolog (DIC-1) produced inviable embryos with increased apoptosis, cavities in cells and abnormal morphogenesis. In the dic-1(RNAi) germ line, ced-3-dependent apoptosis increased, and cell cavities appeared at the late-pachytene/oogenic stage, leading to defective oogenesis. Immunofluorescence microscopy of DIC-1 revealed its ubiquitous expression in the form of cytoplasmic foci, and cryoelectron microscopy narrowed down the location of the foci to the inner membrane of mitochondria. After dic-1 RNAi, mitochondria had an irregular morphology and contained numerous internal vesicles. Homozygous embryos from a heterozygous dic-1 mother arrested at the L3 larval stage, in agreement with the essential role of DIC-1 in mitochondria. In summary, C. elegans DIC-1 plays a crucial role in the formation of normal morphology of the mitochondrial cristae/inner membrane. Our results suggest that human DICE1 may have several functions in multiple intracellular locations.

Original languageEnglish
Pages (from-to)3597-3606
Number of pages10
Issue number18
Publication statusPublished - 2006 Sept


  • Apoptosis
  • C. elegans
  • Cristae remodeling
  • DICE1(INTS6)
  • Mitochondria

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology


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