Wheat gene for all seasons.

Diverse seasonal flowering behaviors drive global adaption of bread wheat (Triticum aestivum), the major crop grown in temperate zones worldwide. Many wheats are sown in autumn and flower only after experiencing the prolonged cold of winter (vernalization). By delaying flowering until spring, the requirement for vernalization minimizes the risk that frost-sensitive flowers and developing grain will be damaged by freezing. This flowering behavior is important in regions where crops are sown in autumn and experience cold winters. In other regions, warm climates, or where crops are sown in spring, the need for cold to stimulate flowering limits wheat cultivation. To adapt wheats to these regions, genes that reduce the vernalization requirement have been used to breed varieties that flower without vernalization. Previous studies have identified the sequences of three of these genes: VERNALIZATION1 (VRN1), VRN2, and VRN3 (1–5). In PNAS, Kippes et al. (6) identify the gene sequence of VRN4, a fourth gene controlling the vernalization requirement of wheat. The authors show that VRN4 is a translocated copy of the VRN1 gene. VRN1 encodes a MADS box (MCM1/ AGAMOUS/DEFICIENS/SRF) transcription factor (1–3). In vernalization-requiring “winter wheats,” VRN1 is transcriptionally activated by prolonged cold to trigger flowering. “Spring wheats” that flower without vernalization typically carry alleles of VRN1 that are actively transcribed without cold, which reduce or eliminate the requirement for vernalization. Kippes et al. (6) show that VRN4 is a variation on this theme: an additional copy of VRN1 that is transcribed without prior cold treatment (Fig. 1). A loss-of-function mutation in the extra copy of VRN1 restores the vernalization requirement, demonstrating that this additional copy of VRN1 corresponds to the VRN4 gene (6). VRN4 occurs widely in an ancient South Asian wheat subspecies, T. aestivum ssp. sphaerococcum, where the extra copy of VRN1 might have originated (6). The reason why the extra copy of VRN1 is active without prior cold exposure is not clear. One possibility is that mutations in the extra copy of VRN1 disrupt the binding site of a RNA binding repressor protein (7). Another possibility is that the new chromosomal location might influence transcriptional activity of the translocated gene copy. Further studies are needed to resolve these possibilities. The study by Kippes et al. (6) further highlights the importance of VRN1 as a regulator of vernalization and as a major gene controlling adaptation and life cycle strategies of wheat. A range of different alleles of VRN1 have been identified in cereal breeding programs (8). It seems likely that further diversity in VRN1 awaits characterization and that this diversity can be harnessed for wheat breeding. Screening for direct regulatory targets of VRN1 has provided insights into a broader genetic network controlling flowering in wheat (9). Similarly, transcriptional regulation of VRN1 activity has been investigated (10–12). There is now great potential to investigate how VRN1 is activated by the cold Fig. 1. Origin of the wheat VRN4 gene that reduces the vernalization requirement. (A) Ancestral hexaploid genome of bread wheat (T. aestivum) had three homeologous VRN1 genes, one on the long arm of chromosome 5 for each of the A, B, and D genomes. VRN1 is a promoter of flowering, but the VRN1 genes are not transcribed until plants experience prolonged cold (vernalization), so flowering is delayed. In this figure, the haploid equivalent is shown, and, normally, there are six copies per nucleus (i.e., AABBDD). (B) VRN1 gene translocated from the long arm of chromosome 5 (A genome) to the centromeric region of chromosome 5 (D genome, proximal region of short arm). The additional VRN1 gene on chromosome 5D has increased transcriptional activity and triggers flowering without vernalization. This extra copy of the VRN1 gene is the basis for the VRN4 gene. Author contributions: B.T. wrote the paper.