Misexpression of a transcriptional repressor candidate provides a molecular mechanism for the suppression of awns by Tipped 1 in wheat

Abstract Awns are bristle-like structures formed at the tip of the lemma on the florets of some cereal grasses. Wild-type wheat is awned, but awnletted and awnless variants have been selected and nowadays all forms are cultivated. In this study, we dissected the genetic control underlying variation...

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Veröffentlicht in:Journal of experimental botany 2020-06, Vol.71 (12), p.3428-3436
Hauptverfasser: Würschum, Tobias, Jähne, Felix, Phillips, Andrew L, Langer, Simon M, Longin, C Friedrich H, Tucker, Matthew R, Leiser, Willmar L
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Sprache:eng
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Zusammenfassung:Abstract Awns are bristle-like structures formed at the tip of the lemma on the florets of some cereal grasses. Wild-type wheat is awned, but awnletted and awnless variants have been selected and nowadays all forms are cultivated. In this study, we dissected the genetic control underlying variation of this characteristic feature by association mapping in a large panel of 1110 winter wheat cultivars of worldwide origin. We identified the B1 (Tipped 1) locus on chromosome 5A as the major determinant of awnlessness globally. Using a combination of fine-mapping and expression analysis, we identified a putative C2H2 zinc finger protein with an EAR domain, characteristic of transcriptional repressors, as a likely candidate for Tipped 1. This gene was found to be up-regulated in awnless B1 compared with awned b1 plants, indicating that misexpression of this transcriptional regulator may contribute to the reduction of awn length in B1 plants. Taken together, our study provides an entry point towards a better molecular understanding of the evolution of morphological features in cereals through selection and breeding. We identified a candidate for the awnedness inhibitor Tipped 1, and showed that misexpression of this transcriptional repressor is the likely molecular cause underlying the evolution of awnlessness in wheat.
ISSN:0022-0957
1460-2431
1460-2431
DOI:10.1093/jxb/eraa106