Maternal microbes support fetal brain wiring

3 min read Original article ↗
  • NEWS AND VIEWS

Resident bacteria in the maternal gut are important for normal fetal brain development in mice. It emerges that this effect is driven by bacterially produced metabolite molecules that signal to the fetal brain.

By

  1. Katherine R. Meckel

    1. Katherine R. Meckel is in the Nash Family Department of Neuroscience and the Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA.

  2. Drew D. Kiraly

    1. Drew D. Kiraly is in the Nash Family Department of Neuroscience and the Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA.

The population of resident gut microorganisms, which are often referred to as the gut microbiota, are crucial for health throughout life. Many studies in animals indicate that the microbiota has a key role in ensuring proper fetal development in the face of environmental stressors. However, what contributions maternal microbes might make to embryo development in the absence of such stressors remain poorly understood. Writing in Nature, Vuong et al.1 report that, in pregnant mice, specific maternal gut bacteria produce molecules as metabolic by-products that influence the neural development of certain sensory pathways in the fetus, leading to lasting behavioural changes in offspring.

Access options

Access Nature and 54 other Nature Portfolio journals

Get Nature+, our best-value online-access subscription

$32.99 / 30 days

cancel any time

Subscribe to this journal

Receive 51 print issues and online access

$199.00 per year

only $3.90 per issue

Rent or buy this article

Prices vary by article type

from$1.95

to$39.95

Prices may be subject to local taxes which are calculated during checkout

Nature 586, 203-205 (2020)

doi: https://doi.org/10.1038/d41586-020-02657-y

References

  1. Vuong, H. E. et al. Nature 586, 281–286 (2020).

    Article  Google Scholar 

  2. Kim, S. et al. Nature 549, 528–532 (2017).

    Article  PubMed  Google Scholar 

  3. Buffington, S. A. et al. Cell 165, 1762–1775 (2016).

    Article  PubMed  Google Scholar 

  4. Jašarević, E. et al. Nature Neurosci. 21, 1061–1071 (2018).

    Article  PubMed  Google Scholar 

  5. Visconti, A. et al. Nature Commun. 10, 4505 (2019).

    Article  PubMed  Google Scholar 

  6. Vojinovic, D. et al. Nature Commun. 10, 5813 (2019).

    Article  PubMed  Google Scholar 

Download references

Subjects

Latest on: