Coupling of Rigor Mortis and Intestinal Necrosis during C. elegans Organismal Death

Cell Rep. 2018 Mar 6;22(10):2730-2741. doi: 10.1016/j.celrep.2018.02.050.

Abstract

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 Ca2+ 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 Ca2+ influx promotes muscle hyper-contraction. In contrast to mammals, DC is an early rather than a late event in C. elegans organismal death. VIDEO ABSTRACT.

Keywords: ATP; C. elegans; aging; calcium; muscle; necrosis; organismal death; pathology; rigor mortis.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine Triphosphate / metabolism
  • Aging / pathology
  • Animals
  • Caenorhabditis elegans / physiology*
  • Caenorhabditis elegans Proteins / genetics
  • Calcium Signaling
  • Death
  • Fluorescence
  • Insulin / metabolism
  • Insulin-Like Growth Factor I / metabolism
  • Intestines / pathology*
  • Models, Biological
  • Muscle Contraction
  • Muscles / pathology
  • Mutation / genetics
  • Necrosis
  • Receptor, Insulin / genetics
  • Rigor Mortis / pathology*

Substances

  • Caenorhabditis elegans Proteins
  • Insulin
  • Insulin-Like Growth Factor I
  • Adenosine Triphosphate
  • DAF-2 protein, C elegans
  • Receptor, Insulin