# Unexpected loss of TAS1R1–TAS1R3 umami taste receptor function in carnivorous Lyncodontini mustelids

**Authors:** Mieczyslaw Wolsan, Jun J Sato

PMC · DOI: 10.1093/chemse/bjaf045 · Chemical Senses · 2025-10-23

## TL;DR

This paper reveals that a taste receptor for savory flavors is nonfunctional in certain weasels and grisons, likely due to their ancestors' diet shift to aquatic prey.

## Contribution

The study identifies a loss of umami taste receptor function in Lyncodontini mustelids, linking it to a historical shift in diet.

## Key findings

- The TAS1R1–TAS1R3 umami taste receptor is nonfunctional in all Lyncodontini species.
- The receptor loss occurred in the stem lineage of Lyncodontini around 3 to 9.5 million years ago.
- The loss is hypothesized to be linked to a semiaquatic diet rich in fish and invertebrates low in umami compounds.

## Abstract

Lyncodon patagonicus (Patagonian weasel), Galictis cuja (lesser grison), and Galictis vittata (greater grison) are the only extant species of Lyncodontini, a relatively poorly known Neotropical tribe of the mustelid subfamily Ictonychinae within the mammalian order Carnivora. Here, we report molecular evidence indicating that the TAS1R1–TAS1R3 umami (savory) taste receptor lost its function in the Lyncodontini's stem lineage (∼3 to 9.5 million years ago) and is therefore nonfunctional in all crown Lyncodontini. This finding is unexpected and intriguing because all extant Lyncodontini apparently need this receptor (they are terrestrial carnivores with diets high in umami-eliciting compounds, including purine 5′-monophosphate ribonucleotides, the main agonists of TAS1R1–TAS1R3 in carnivorans). We argue that the common ancestor of extant Lyncodontini that first lost TAS1R1–TAS1R3 function was semiaquatic and predated mainly on fish and/or aquatic invertebrates (tissues of living or recently dead fish and aquatic invertebrates are low in purine 5′-monophosphate ribonucleotides). This hypothesis is consistent with the idea that loss of taste receptor function is caused by feeding specializations that restrict access to the compounds that a particular receptor detects. Our hypothesis effectively suggests a prolonged semiaquatic episode in the evolutionary history of the Lyncodontini's stem lineage because loss of TAS1R1–TAS1R3 function is achieved by a stochastic process continuing over evolutionary time. Whether the extant Lyncodontini evolved a mechanism to compensate for the loss of TAS1R1–TAS1R3 function is currently unknown and requires further research.

## Linked entities

- **Genes:** TAS1R1 (taste 1 receptor member 1) [NCBI Gene 80835], TAS1R3 (taste 1 receptor member 3) [NCBI Gene 83756]
- **Species:** Lyncodon patagonicus (taxon 768574), Galictis cuja (taxon 470561), Galictis vittata (taxon 204265), Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** TAS1R3 (taste 1 receptor member 3) [NCBI Gene 83756] {aka T1R3}, TAS1R1 (taste 1 receptor member 1) [NCBI Gene 80835] {aka GM148, GPR70, T1R1, TR1}
- **Diseases:** greater (MESH:D012784)
- **Chemicals:** purine 5'-monophosphate ribonucleotides (-)
- **Species:** Lyncodon patagonicus (Patagonian weasel, species) [taxon 768574], Galictis cuja (Lesser grison, species) [taxon 470561], Homo sapiens (human, species) [taxon 9606], Galictis vittata (Greater grison, species) [taxon 204265]

## Full text

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## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12596590/full.md

## References

70 references — full list in the complete paper: https://tomesphere.com/paper/PMC12596590/full.md

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Source: https://tomesphere.com/paper/PMC12596590