A WOX homolog disrupted by a transposon led to the loss of spines and contributed to the domestication of lettuce
© 2024 The Authors New Phytologist © 2024 New Phytologist Foundation.
| Veröffentlicht in: | The New phytologist. - 1979. - 242(2024), 6 vom: 27. Juni, Seite 2857-2871 |
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| 1. Verfasser: | |
| Weitere Verfasser: | , , , , , , |
| Format: | Online-Aufsatz |
| Sprache: | English |
| Veröffentlicht: |
2024
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| Zugriff auf das übergeordnete Werk: | The New phytologist |
| Schlagworte: | Journal Article CACTA transposon WS1 domestication lettuce spine DNA Transposable Elements Homeodomain Proteins Plant Proteins |
| Zusammenfassung: | © 2024 The Authors New Phytologist © 2024 New Phytologist Foundation. The loss of spines is one of the most important domestication traits for lettuce (Lactuca sativa). However, the genetics and regulation of spine development in lettuce remain unclear. We examined the genetics of spines in lettuce using a segregating population derived from a cross between cultivated and wild lettuce (Lactuca serriola). A gene encoding WUSCHEL-related homeobox transcription factor, named as WOX-SPINE1 (WS1), was identified as the candidate gene controlling the spine development in lettuce, and its function on spines was verified. A CACTA transposon was found to be inserted into the first exon of the ws1 allele, knocking out its function and leading to the lack of spines in cultivated lettuce. All lettuce cultivars investigated have the nonfunctional ws1 gene, and a selection sweep was found at the WS1 locus, suggesting its important role in lettuce domestication. The expression levels of WS1 were associated with the density of spines among different accessions of wild lettuce. At least two independent loss-of-function mutations in the ws1 gene caused the loss of spines in wild lettuce. These findings provide new insights into the development of spines and facilitate the exploitation of wild genetic resources in future lettuce breeding programs |
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| Beschreibung: | Date Completed 23.05.2024 Date Revised 29.07.2024 published: Print-Electronic RefSeq: OQ858569 Citation Status MEDLINE |
| ISSN: | 1469-8137 |
| DOI: | 10.1111/nph.19738 |