Format

Send to

Choose Destination
Cell Host Microbe. 2014 Oct 8;16(4):495-503. doi: 10.1016/j.chom.2014.09.001. Epub 2014 Sep 25.

Discovery and characterization of gut microbiota decarboxylases that can produce the neurotransmitter tryptamine.

Author information

1
Department of Bioengineering and Therapeutic Sciences and the California Institute for Quantitative Biosciences, University of California, San Francisco, San Francisco, CA 94158, USA.
2
ETH Zurich, Institute of Molecular Systems Biology, Zurich 8093, Switzerland.
3
Faculty of Agriculture, Tottori University, Koyama, Tottori 680-8550, Japan.
4
Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA.
5
Department of Bioengineering and Therapeutic Sciences and the California Institute for Quantitative Biosciences, University of California, San Francisco, San Francisco, CA 94158, USA. Electronic address: fischbach@fischbachgroup.org.

Abstract

Several recent studies describe the influence of the gut microbiota on host brain and behavior. However, the mechanisms responsible for microbiota-nervous system interactions are largely unknown. Using a combination of genetics, biochemistry, and crystallography, we identify and characterize two phylogenetically distinct enzymes found in the human microbiome that decarboxylate tryptophan to form the β-arylamine neurotransmitter tryptamine. Although this enzymatic activity is exceedingly rare among bacteria more broadly, analysis of the Human Microbiome Project data demonstrate that at least 10% of the human population harbors at least one bacterium encoding a tryptophan decarboxylase in their gut community. Our results uncover a previously unrecognized enzymatic activity that can give rise to host-modulatory compounds and suggests a potential direct mechanism by which gut microbiota can influence host physiology, including behavior.

PMID:
25263219
PMCID:
PMC4260654
DOI:
10.1016/j.chom.2014.09.001
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center