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<p>Nutritional effects on trait inheritance are widespread in animals including human famines, representing some of the most severe environmental influences on organismal phenotypes and can be transmitted over generations. However, the chemical nature of the stimuli inducing such memory remains elusive. The nematode <i>Pristionchus pacificus</i> exhibits mouth-form plasticity including predation and responds to a multigenerational <i>Novosphingobium</i> diet with the induction and transgenerational inheritance of the predatory morph. We show that bacteria-derived vitamin B12 is necessary and sufficient for transgenerational memory. <i>Novosphingobium</i> mutants defective in vitamin B12 production do not induce transgenerational inheritance, but vitamin B12 supplementation can rescue the memory phenotype. Different vitamin B12 concentrations are required for the original induction and subsequent transgenerational inheritance of the predatory morph. This inherited effect acts through increased multigenerational vitellogenin transcription suggesting elevated nutrient provisioning. Consistently, mutants in the vitellogenin receptor <i>Ppa-rme-2</i> are memory-defective indicating that a vitamin acts through maternal provisioning to progeny. Thus, vitamin B12 induces vitellogenin provisioning to control organismal physiology and behavior.</p>

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Vitamin B12 induces memory of predation through vitellogenin provisioning

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月9日

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  • Shiela Pearl Quiobe,
  • Ata Kalirad,
  • Raphaela Zurheide,
  • Hanh Witte,
  • Christian Rödelsperger,
  • Ralf J. Sommer

摘要

Nutritional effects on trait inheritance are widespread in animals including human famines, representing some of the most severe environmental influences on organismal phenotypes and can be transmitted over generations. However, the chemical nature of the stimuli inducing such memory remains elusive. The nematode Pristionchus pacificus exhibits mouth-form plasticity including predation and responds to a multigenerational Novosphingobium diet with the induction and transgenerational inheritance of the predatory morph. We show that bacteria-derived vitamin B12 is necessary and sufficient for transgenerational memory. Novosphingobium mutants defective in vitamin B12 production do not induce transgenerational inheritance, but vitamin B12 supplementation can rescue the memory phenotype. Different vitamin B12 concentrations are required for the original induction and subsequent transgenerational inheritance of the predatory morph. This inherited effect acts through increased multigenerational vitellogenin transcription suggesting elevated nutrient provisioning. Consistently, mutants in the vitellogenin receptor Ppa-rme-2 are memory-defective indicating that a vitamin acts through maternal provisioning to progeny. Thus, vitamin B12 induces vitellogenin provisioning to control organismal physiology and behavior.