4.7 Article

Deciphering the complex nature of bolting time regulation in Beta vulgaris

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THEORETICAL AND APPLIED GENETICS
卷 130, 期 8, 页码 1649-1667

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SPRINGER
DOI: 10.1007/s00122-017-2916-2

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  1. priority program of the German Research Foundation (DFG) [SPP 1530, TR 1088/1-1]

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Only few genetic loci are sufficient to increase the variation of bolting time in Beta vulgaris dramatically, regarding vernalization requirement, seasonal bolting time and reproduction type. Beta species show a wide variation of bolting time regarding the year of first reproduction, seasonal bolting time and the number of reproduction cycles. To elucidate the genetics of bolting time control, we used three F-3 mapping populations that were produced by crossing a semelparous, annual sugar beet with iteroparous, vernalization-requiring wild beet genotypes. The semelparous plants died after reproduction, whereas iteroparous plants reproduced at least twice. All populations segregated for vernalization requirement, seasonal bolting time and the number of reproduction cycles. We found that vernalization requirement co-segregated with the bolting locus B on chromosome 2 and was inherited independently from semel- or iteroparous reproduction. Furthermore, we found that seasonal bolting time is a highly heritable trait (h (2) > 0.84), which is primarily controlled by two major QTL located on chromosome 4 and 9. Late bolting alleles of both loci act in a partially recessive manner and were identified in both iteroparous pollinators. We observed an additive interaction of both loci for bolting delay. The QTL region on chromosome 4 encompasses the floral promoter gene BvFT2, whereas the QTL on chromosome 9 co-localizes with the BR (1) locus, which controls post-winter bolting resistance. Our findings are applicable for marker-assisted sugar beet breeding regarding early bolting to accelerate generation cycles and late bolting to develop bolting-resistant spring and winter beets. Unexpectedly, one population segregated also for dwarf growth that was found to be controlled by a single locus on chromosome 9.

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