鳥類が甘味を認識する進化的仕組みを解明(How birds achieve sweet success)

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2026-02-26 マックス・プランク研究所

Max Planck Societyの研究チームは、鳥類がどのようにして甘味を感知できるよう進化したのかを解明した。多くの鳥は本来甘味受容体を持たないが、花蜜を主食とする系統では、うま味受容体を構成するタンパク質が変化し、糖を認識できるよう機能転換していたことが分かった。この分子進化により、鳥は花蜜資源を利用できるようになり、植物との共進化が促進された。研究は味覚受容体の可塑性と進化的適応の仕組みを示し、生態学と分子生物学の両面で重要な知見を提供する。

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収束的かつ系統特異的なゲノム変化が砂糖を消費する鳥類の適応を形作る Convergent and lineage-specific genomic changes shape adaptations in sugar-consuming birds

Ekaterina Osipova, Meng-Ching Ko, Konstantin M. Petricek, Simon Yung Wa Sin, […] , and Timothy B. Sackton
Science  Published:26 Feb 2026

Editor’s summary

Diets based primarily on nectar require physiological adaptations to avoid metabolic issues. Osipova et al. generated new genomes for nine bird species as well as transcriptomes of digestion-related tissues for sugar-consuming birds and related outgroups. They particularly looked for signatures of selection shared among these species. Although the authors identified many lineage-specific changes, regulatory and protein-coding changes were shared more broadly for multiple genes involved in the response to sugars. The only gene that showed signs of selection across all sugar-consuming lineages was MLXIPL, which encodes a transcription factor that increases the expression of genes responsible for glucose metabolism and lipogenesis. —Corinne Simonti

Structured Abstract

INTRODUCTION

High sugar consumption in humans is associated with increased risk of type 2 diabetes and other metabolic conditions. However, four independent lineages of birds—hummingbirds, parrots, honeyeaters, and sunbirds—have evolved to rely almost entirely on fruit and nectar, which are food sources that consist primarily of simple sugars. The genomic basis of adaptations to such sugar-rich diets is largely unknown.

RATIONALE

We used comparative genomics and transcriptomics combined with functional validation to address the following questions: (i) What are the main genomic targets of selection in the evolution of high-sugar diets in birds, and (ii) do lineage-specific or repeated molecular changes underlie these convergent adaptations? To address these questions, we generated nine new genomes from five sugar-feeding species and four of their closely related non–sugar-feeding outgroups. We also generated transcriptomes from five metabolically relevant tissues of three sugar-feeding species and three non–sugar-feeding outgroups. Using these and existing genomic resources, we tested for selection in protein-coding and noncoding regions. We also screened for signatures of gene expression evolution between sugar-specialist species and control groups.

RESULTS

We discovered both shared and lineage-specific molecular adaptations in sugar-consuming birds. We found significantly more shared signatures of selection among sugar feeders than non–sugar-specialist control groups. These repeated signals of positive selection occur in protein-coding genes and regulatory elements and target a shared set of pathways across sugar-feeding groups, including major metabolic pathways, such as sugar, lipid, and amino acid metabolism, as well as pathways that in humans are associated with pathologies, such as type 2 diabetes and dysregulated blood pressure. We also found lineage-specific signals of selection, which often represent elaborations of these same pathways, exemplified by functional changes specifically in the honeyeater hexokinase 3 (HK3) protein. The contribution of protein sequence and regulatory evolution differs between pathways. Whereas both protein sequence and regulatory evolution contributed to adaptations in sugar metabolism, adaptations in lipid and amino acid metabolism and blood pressure regulation mainly involved regulatory evolution.

We found that a key transcriptional regulator of sugar and lipid homeostasis, MLXIPL, showed notable evidence of convergence, as it evolved under positive selection and showed regulatory changes in all four sugar-feeding groups. We introduced hummingbird MLXIPL into a human cell line and showed that hummingbird MLXIPL enhances sugar response in cells, highlighting its adaptive role in high-sugar diets.

CONCLUSION

Our findings suggest that both convergent and lineage-specific strategies have played roles in the evolution of adaptations to sugar-rich diets and underscore the complex patterns of repeated molecular changes in both protein-coding loci and regulatory elements in shaping metabolic pathways. This research contributes to the field by (i) elucidating the main genomic targets in the evolution of sugar-feeding and (ii) demonstrating the power of comparative analysis in pinpointing specific genes, regulatory elements, and pathways responsible for complex traits.

鳥類が甘味を認識する進化的仕組みを解明(How birds achieve sweet success)
Our comparative screens across four independent sugar-feeding bird groups identified both repeated and lineage-specific targets of selection.
Our study aimed to understand the genomic changes occurring in groups of birds that have adapted to consume a diet very high in sugars, focusing on four independent transitions to high sugar consumption (left). To identify repeated and lineage-specific signatures of selection associated with this shift, we ran comparative screens in both protein-coding and noncoding genomic regions and analyzed shifts in gene expression (middle). We identified several key pathways repeatedly targeted by selection in independent sugar-feeding groups (right). Functional assays demonstrated that changes in a master regulator of sugar and lipid metabolism, MLXIPL, enhanced sugar response in a model system and validated lineage-specific functional changes in honeyeater HK3 (bottom right). CNEE, conserved non-exonic element; Vmax, maximum velocity.

Abstract

High-sugar diets cause human metabolic diseases, yet several bird lineages convergently adapted to feeding on sugar-rich nectar or fruits. We investigated the underlying molecular mechanisms in hummingbirds, parrots, honeyeaters, and sunbirds by generating nine new genomes and 90 tissue-specific transcriptomes. Comparative screens revealed an excess of repeated selection in both protein-coding and regulatory sequences in sugar-feeding birds, suggesting reuse of genetic elements. Sequence or expression changes in sugar-feeders affect genes involved in blood pressure regulation and lipid, amino acid, and carbohydrate metabolism, with experiments showing functional changes in honeyeater hexokinase 3. MLXIPL, a key regulator of sugar and lipid homeostasis, showed convergent sequence and regulatory changes across all sugar-feeding clades; experiments revealed enhanced sugar-induced transcriptional activity of hummingbird MLXIPL, highlighting its adaptive role in high-sugar diets.

細胞遺伝子工学
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