Cell-nonautonomous inhibition of radiation-induced apoptosis by dynein light chain 1 in Caenorhabditis elegans

T H Morthorst, A Olsen

Research output: Contribution to journalJournal articleResearchpeer-review

8 Citations (Scopus)


The evolutionarily conserved process of programmed cell death, apoptosis, is essential for development of multicellular organisms and is also a protective mechanism against cellular damage. We have identified dynein light chain 1 (DLC-1) as a new regulator of germ cell apoptosis in Caenorhabditis elegans. The DLC-1 protein is highly conserved across species and is a part of the dynein motor complex. There is, however, increasing evidence for dynein-independent functions of DLC-1, and our data describe a novel dynein-independent role. In mammalian cells, DLC-1 is important for cellular transport, cell division and regulation of protein activity, and it has been implicated in cancer. In C. elegans, we find that knockdown of dlc-1 by RNA interference (RNAi) induces excessive apoptosis in the germline but not in somatic cells during development. We show that DLC-1 mediates apoptosis through the genes lin-35, egl-1 and ced-13, which are all involved in the response to ionising radiation (IR)-induced apoptosis. In accordance with this, we show that IR cannot further induce apoptosis in dlc-1(RNAi) animals. Furthermore, we find that DLC-1 is functioning cell nonautonomously through the same pathway as kri-1 in response to IR-induced apoptosis and that DLC-1 regulates the levels of KRI-1. Our results strengthen the notion of a highly dynamic communication between somatic cells and germ cells in regulating the apoptotic process.

Original languageEnglish
JournalCell Death & Disease
Pages (from-to)e799
Publication statusPublished - 12 Sept 2013
Externally publishedYes


  • Animals
  • Animals, Genetically Modified
  • Apoptosis/radiation effects
  • Caenorhabditis elegans/cytology
  • Caenorhabditis elegans Proteins/metabolism
  • Dyneins/metabolism
  • Germ Cells/cytology
  • Green Fluorescent Proteins/metabolism
  • Models, Biological
  • Radiation, Ionizing


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