Plant Breeding Institute, University of Kiel, Am Botanischen Garten 1-9, 24118, Kiel, Germany.
Leibniz Institute of Vegetable and Ornamental Crops, Kühnhäuser Straße 101, 99090, Erfurt, Germany.
Theor Appl Genet. 2017 Aug;130(8):1649-1667. doi: 10.1007/s00122-017-2916-2. Epub 2017 May 6.
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 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 > 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 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.
仅有少数几个遗传基因座就足以极大地增加糖用甜菜开花时间的变异性，包括春化需求、季节性开花时间和繁殖类型。不同的糖用甜菜品种在首次繁殖的年份、季节性开花时间和繁殖周期的数量上表现出开花时间的广泛变异性。为了阐明开花时间控制的遗传学基础，我们使用了三个 F 作图群体，这些群体是通过杂交半常绿、一年生的糖用甜菜与常绿、需要春化的野生甜菜基因型产生的。半常绿植物在繁殖后死亡，而常绿植物至少繁殖两次。所有群体都在春化需求、季节性开花时间和繁殖周期的数量上发生分离。我们发现春化需求与染色体 2 上的开花基因座 B 共分离，并且与半常绿或常绿繁殖是独立遗传的。此外，我们发现季节性开花时间是一个高度可遗传的性状（h > 0.84），主要由位于染色体 4 和 9 上的两个主要 QTL 控制。这两个基因座的晚开花等位基因以部分隐性方式作用，并且在常绿授粉者中都被鉴定出来。我们观察到这两个基因座的延迟开花存在加性互作。染色体 4 上的 QTL 区域包含花启动子基因 BvFT2，而染色体 9 上的 QTL 与控制冬季后开花抗性的 BR 基因座共定位。我们的研究结果适用于标记辅助甜菜育种，以促进早期开花，加速世代周期，以及培育抗春化和抗冬季的甜菜。出乎意料的是，一个群体也分离出矮化生长，这是由染色体 9 上的一个单一基因座控制的。
