Send to

Choose Destination
Nat Commun. 2015 Jul 14;6:7618. doi: 10.1038/ncomms8618.

Gut microbiota mediate caffeine detoxification in the primary insect pest of coffee.

Author information

Ecology Department, Earth Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA.
Sustainable Perennial Crops Laboratory, United States Department of Agriculture, Agricultural Research Service, Building 001, BARC-W, Beltsville, Maryland 20705, USA.
Genome Dynamics Department, Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA.
International Maize and Wheat Improvement Center (CIMMYT), Carretera Mexico-Veracruz Km. 45, El Batán, Texcoco 56130, Mexico.
El Colegio de la Frontera Sur (ECOSUR), Carretera Antiguo Aeropuerto Km. 2.5, Tapachula, Chiapas 30700, Mexico.
Department of Environmental Science, Policy and Management, University of California, Berkeley, California 94720, USA.


The coffee berry borer (Hypothenemus hampei) is the most devastating insect pest of coffee worldwide with its infestations decreasing crop yield by up to 80%. Caffeine is an alkaloid that can be toxic to insects and is hypothesized to act as a defence mechanism to inhibit herbivory. Here we show that caffeine is degraded in the gut of H. hampei, and that experimental inactivation of the gut microbiota eliminates this activity. We demonstrate that gut microbiota in H. hampei specimens from seven major coffee-producing countries and laboratory-reared colonies share a core of microorganisms. Globally ubiquitous members of the gut microbiota, including prominent Pseudomonas species, subsist on caffeine as a sole source of carbon and nitrogen. Pseudomonas caffeine demethylase genes are expressed in vivo in the gut of H. hampei, and re-inoculation of antibiotic-treated insects with an isolated Pseudomonas strain reinstates caffeine-degradation ability confirming their key role.

[Indexed for MEDLINE]
Free PMC Article

Publication types, MeSH terms, Substances, Secondary source ID

Publication types

MeSH terms


Secondary source ID

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center