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Fungal pathogens and symbionts: Living off the fat of the land

Summary

Certain fungi that live exclusively in or on hosts have evolved a clever survival strategy: they stopped making their own fatty acids and instead steal them from their hosts. This includes fungi that cause pneumonia in immunocompromised patients, yeasts on skin, and beneficial fungi that help plants absorb nutrients from soil. By examining how these fungi scavenge fatty acids from their hosts, scientists hope to develop better treatments and diagnostic tools for fungal infections.

Background

Fatty acid synthesis is essential for free-living fungi and represents an energetically costly process. However, several evolutionarily divergent fungal species that have developed obligate relationships with their hosts have independently lost the capacity to synthesize fatty acids de novo, instead relying on host-derived fatty acids for survival and growth.

Objective

This review discusses the independent loss of de novo fatty acid biosynthetic capacity in fungal species including Pneumocystis, Malassezia, Microsporidia, and arbuscular mycorrhizal fungi (AMF), examining the evolutionary convergence and metabolic mechanisms underlying this adaptation to obligate host relationships.

Results

Multiple fungal pathogens and symbionts have convergently lost FAS genes despite being evolutionarily divergent: Pneumocystis species lack FAS1 and FAS2 genes, Malassezia species lack cytosolic FAS genes, Microsporidia have highly reduced genomes lacking FAS, and AMF have lost FAS genes. These fungi employ various mechanisms to acquire fatty acids from hosts, including transporter proteins and endocytosis.

Conclusion

The independent loss of fatty acid synthesis capacity in diverse fungal species represents a convergent evolutionary strategy that reflects adaptation to fatty acid-rich host environments. Understanding these mechanisms is crucial for developing better diagnostics, vaccines, and antifungal therapies, though cultivation challenges remain significant obstacles to research.
  • Published in:PLoS Pathogens,
  • Study Type:Review,
  • Source: 10.1371/journal.ppat.1012551, PMID: 39325846
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