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Food and metabolic signalling defects in a Caenorhabditis elegans serotonin-synthesis mutant

Author

Listed:
  • Ji Ying Sze

    (Massachusetts General Hospital, Harvard Medical School
    University of California)

  • Martin Victor

    (Harvard Medical School)

  • Curtis Loer

    (University of San Diego)

  • Yang Shi

    (Harvard Medical School)

  • Gary Ruvkun

    (Massachusetts General Hospital, Harvard Medical School)

Abstract

The functions of serotonin have been assigned through serotonin-receptor-specific drugs and mutants1,2; however, because a constellation of receptors remains when a single receptor subtype is inhibited, the coordinate responses to modulation of serotonin levels may be missed. Here we report the analysis of behavioural and neuroendocrine defects caused by a complete lack of serotonin signalling. Analysis of the C. elegans genome sequence showed that there is a single tryptophan hydroxylase gene (tph-1)—the key enzyme for serotonin biosynthesis. Animals bearing a tph-1 deletion mutation do not synthesize serotonin but are fully viable. The tph-1 mutant shows abnormalities in behaviour and metabolism that are normally coupled with the sensation and ingestion of food: rates of feeding and egg laying are decreased; large amounts of fat are stored; reproductive lifespan is increased; and some animals arrest at the metabolically inactive dauer stage. This metabolic dysregulation is, in part, due to downregulation of tranforming growth factor-β and insulin-like neuroendocrine signals. The action of the C. elegans serotonergic system in metabolic control is similar to mammalian serotonergic input to metabolism and obesity2.

Suggested Citation

  • Ji Ying Sze & Martin Victor & Curtis Loer & Yang Shi & Gary Ruvkun, 2000. "Food and metabolic signalling defects in a Caenorhabditis elegans serotonin-synthesis mutant," Nature, Nature, vol. 403(6769), pages 560-564, February.
    • Handle: RePEc:nat:nature:v:403:y:2000:i:6769:d:10.1038_35000609
    DOI: 10.1038/35000609
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    Cited by:

    1. Tripti Nair & Brandy A. Weathers & Nicole L. Stuhr & James D. Nhan & Sean P. Curran, 2024. "Serotonin deficiency from constitutive SKN-1 activation drives pathogen apathy," Nature Communications, Nature, vol. 15(1), pages 1-14, December.
    2. Mikaeli Anne Carmichael & Rebecca Louise Thomson & Lisa Jane Moran & Thomas Philip Wycherley, 2021. "The Impact of Menstrual Cycle Phase on Athletes’ Performance: A Narrative Review," IJERPH, MDPI, vol. 18(4), pages 1-24, February.
    3. Rebecca Cornell & Wei Cao & Bernie Harradine & Rasoul Godini & Ava Handley & Roger Pocock, 2024. "Neuro-intestinal acetylcholine signalling regulates the mitochondrial stress response in Caenorhabditis elegans," Nature Communications, Nature, vol. 15(1), pages 1-12, December.
    4. Ria S. Peesapati & Brianna L. Austin-Byler & Fathima Zahra Nawaz & Jonathan B. Stevenson & Stanelle A. Mais & Rabia N. Kaya & Michael G. Hassan & Nabraj Khanal & Alexandra C. Wells & Deena Ghiai & Ani, 2024. "A specific folate activates serotonergic neurons to control C. elegans behavior," Nature Communications, Nature, vol. 15(1), pages 1-16, December.
    5. Hillary A. Miller & Shijiao Huang & Elizabeth S. Dean & Megan L. Schaller & Angela M. Tuckowski & Allyson S. Munneke & Safa Beydoun & Scott D. Pletcher & Scott F. Leiser, 2022. "Serotonin and dopamine modulate aging in response to food odor and availability," Nature Communications, Nature, vol. 13(1), pages 1-13, December.

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