The causal mutation leading to sweetness in modern white lupin cultivars

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Lupins are high-protein crops that are rapidly gaining interest as hardy alternatives to soybean; however, they accumulate antinutritional alkaloids of the quinolizidine type (QAs). Lupin domestication was enabled by the discovery of genetic loci conferring low QA levels (sweetness), but the precise identity of the underlying genes remains uncertain. We show that pauper, the most common sweet locus in white lupin, encodes an acetyltransferase (AT) unexpectedly involved in the early QA pathway. In pauper plants, a single-nucleotide polymorphism (SNP) strongly impairs AT activity, causing pathway blockage. We corroborate our hypothesis by replicating the pauper chemotype in narrow-leafed lupin via mutagenesis. Our work adds a new dimension to QA biosynthesis and establishes the identity of a lupin sweet gene for the first time, thus facilitating lupin breeding and enabling domestication of other QA-containing legumes.

TidsskriftScience Advances
Udgave nummer31
Antal sider10
StatusUdgivet - 2023

Bibliografisk note

Funding Information:
This work was supported by the VILLUM Foundation project 15476 (D.M., H.G.G., and F.G.-F.), the Novo Nordisk Foundation project NNF2019OC53580 (D.M., H.G.G., and F.G.-F.), the Polish Ministry of Agriculture and Rural Development Multiannual Programme RM-111-222-15 (K.C. and M.K.), Innovate UK project 133048 (J.L.T., L.Y., and M.N.N.), and the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation program Starting Grant LUPINROOTS grant agreement no. 637420 (B.H. and B.P.).

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Copyright © 2023 The Authors, some rights reserved.

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