# Bacterial partners as a mode of fungal resistance to antimicrobial compounds

> **NIH NIH R35** · UNIVERSITY OF GEORGIA · 2023 · $368,444

## Abstract

Project Summary
The species composition of microbial communities determines the impact they have on human health and the
environment, but we have a very limited understanding of how microbial communities form. A major driver of
this composition is a competition among microbes that is mediated by naturally produced antimicrobial
compounds, that help shape which microbes are included or excluded from the community. Notably, many key
microbes found in these communities are sensitive to the natural antimicrobial compounds produced therein.
This is especially true for fungi, which are particularly vulnerable to many classes of toxic antifungal
compounds produced within microbial communities. Despite this, fungi play key roles in host-associated
microbial communities for plants, animals, and humans. In order to explain how such sensitive organisms gain
access to antimicrobial replete spaces, my lab discovered a class of microbial interactions whereby bacterial
members of the community that are resistant to antimicrobial compounds extend protection to physically
associated fungal partners. Such bacterial partners act as “toxin sponges,” sequestering natural antimicrobial
compounds, in addition to providing protection against frontline antifungal drugs used clinically against fungal
pathogens. The discovery of bacterial partners protecting their host fungi provides an unstudied avenue that
can be applied to A) predicting how microbial communities form and B) dissecting new mechanisms of
resistance to antifungal drugs whereby resistance originates from a bacterial partner.
My lab focuses on developing a model system based on this type of symbiosis, making use of a co-isolated
fungal-bacterial pairing. The fungus, Aspergillus calidoustus, was found physically associated with a novel
bacterium we named Paraburkholderia edwinii. We have rendered the bacterium genetically tractable and are
working to do the same with the fungus. We are interested in discovering the mechanisms at work for
protection on three levels. First, at the level of the bacterium, we are characterizing how the bacterium
processes and detoxifies antifungal compounds. Second, at the level of the bacterial-fungal interface, we are
interested in understanding how signals of fungal stress are communicated to the bacterium to activate the
protection response. Finally, at the level of the mixed bacterial-fungal co-colony, we are focused on
understanding how antifungal drug flow is manipulated through the fungal mycelial structure to bacterial
aggregates that form within where detoxification of the drugs occurs. Beyond the mechanisms involved in this
pairing, we aim to co-isolate bacterial-fungal pairs from clinical samples to identify which bacterial members of
microbial communities provide safe harbor for associated fungi, and to what classes of antifungal compounds
such partnerships can defend against.

## Key facts

- **NIH application ID:** 10714362
- **Project number:** 1R35GM150797-01
- **Recipient organization:** UNIVERSITY OF GEORGIA
- **Principal Investigator:** Kurt M. Dahlstrom
- **Activity code:** R35 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2023
- **Award amount:** $368,444
- **Award type:** 1
- **Project period:** 2023-07-01 → 2028-04-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10714362

## Citation

> US National Institutes of Health, RePORTER application 10714362, Bacterial partners as a mode of fungal resistance to antimicrobial compounds (1R35GM150797-01). Retrieved via AI Analytics 2026-05-27 from https://api.ai-analytics.org/grant/nih/10714362. Licensed CC0.

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