Ferritin is regulated by a neuro-intestinal axis in the nematode Caenorhabditis elegans

Leonor Romero-Afrima, Veronica Zelmanovich, Zohar Abergel, Binyamin Zuckerman, Maayan Shaked, Rachel Abergel, Leonid Livshits, Yoav Smith, Einav Gross*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

9 Scopus citations

Abstract

Iron is vital for the life of most organisms. However, when dysregulated, iron can catalyze the formation of oxygen (O2) radicals that can destroy any biological molecule and thus lead to oxidative injury and death. Therefore, iron metabolism must be tightly regulated at all times, as well as coordinated with the metabolism of O2. However, how is this achieved at the whole animal level is not well understood. Here, we explore this question using the nematode Caenorhabditis elegans. Exposure of worms to O2 starvation conditions (i.e. hypoxia) induces a major upregulation in levels of the conserved iron-cage protein ferritin 1 (ftn-1) in the intestine, while exposure to 21% O2 decreases ftn-1 level. This O2-dependent inhibition is mediated by O2-sensing neurons that communicate with the intestine through neurotransmitter and neuropeptide signalling, and requires the activity of hydroxylated HIF-1. By contrast, the induction of ftn-1 in hypoxia appears to be HIF-1-independent. This upregulation provides protection against Pseudomonas aeruginosa bacteria and oxidative injury. Taken together, our studies uncover a neuro-intestine axis that coordinates O2 and iron responses at the whole animal level.

Original languageAmerican English
Article number101359
JournalRedox Biology
Volume28
DOIs
StatePublished - Jan 2020

Bibliographical note

Publisher Copyright:
© 2019 The Authors

Keywords

  • Caenorhabditis elegans
  • EGL-9
  • Ferritin
  • HIF-1
  • Hypoxia
  • Oxygen sensing neurons
  • Soluble guanylate cyclases
  • VHL-1
  • ftn-1

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