Organismal death is a process of systemic collapse whose mechanisms are less well understood than those of cell death. We previously reported that death in C. elegans is accompanied by a calcium-propagated wave of intestinal necrosis, marked by a wave of blue autofluorescence (death fluorescence). Here, we describe another feature of organismal death, a wave of body wall muscle contraction, or death contraction (DC). This phenomenon is accompanied by a wave of intramuscular Ca 2+ release and, subsequently, of intestinal necrosis. Correlation of directions of the DC and intestinal necrosis waves implies coupling of these death processes. Long-lived insulin/IGF-1-signaling mutants show reduced DC and delayed intestinal necrosis, suggesting possible resistance to organismal death. DC resembles mammalian rigor mortis, a postmortem necrosis-related process in which Ca 2+ influx promotes muscle hyper-contraction. In contrast to mammals, DC is an early rather than a late event in C. elegans organismal death.

Introduction

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Here we describe the occurrence of a rigor mortis-like process in C. elegans. We report that a transient reduction in body length occurs during death in young adult worms killed using lethal stress and during death from old age. We show that such death contraction is altered by manipulations of muscle function in a manner consistent with the occurrence of rigor mortis during C. elegans organismal death. Death contraction also precedes, and is coupled with, intestinal necrosis. This suggests that an organism-wide wave of Ca2+ release causes rigor mortis and intestinal necrosis and is a major event driving organismal death in C. elegans. We also find that death contraction is suppressed in long-lived daf-2 insulin/IGF-1 receptor mutants, suggesting possible organismal death resistance, and that this suppression requires daf-18/PTEN, but not daf-16/FoxO.