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Mutation of a bHLH transcription factor allowed almond domestication

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Science  14 Jun 2019:
Vol. 364, Issue 6445, pp. 1095-1098
DOI: 10.1126/science.aav8197

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How to make almonds palatable

The domesticated almond tree has been feeding humans for millennia. Derivation from the wild, bitter, and toxic almond required loss of the cyanogenic diglucoside amygdalin. Sánchez-Pérez et al. sequenced the almond genome and analyzed the genomic region responsible for this shift. The key change turned out to be a point mutation in a transcription factor that regulates production of P450 monooxygenases in the biosynthetic pathway for the toxic compound.

Science, this issue p. 1095

Abstract

Wild almond species accumulate the bitter and toxic cyanogenic diglucoside amygdalin. Almond domestication was enabled by the selection of genotypes harboring sweet kernels. We report the completion of the almond reference genome. Map-based cloning using an F1 population segregating for kernel taste led to the identification of a 46-kilobase gene cluster encoding five basic helix-loop-helix transcription factors, bHLH1 to bHLH5. Functional characterization demonstrated that bHLH2 controls transcription of the P450 monooxygenase–encoding genes PdCYP79D16 and PdCYP71AN24, which are involved in the amygdalin biosynthetic pathway. A nonsynonymous point mutation (Leu to Phe) in the dimerization domain of bHLH2 prevents transcription of the two cytochrome P450 genes, resulting in the sweet kernel trait.

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