Most of the natural variation in wheat vernalization response is determined by allelic differences in the MADS-box transcription factor VERNALIZATION1 (VRN1). Extended exposures to low temperatures during the winter (vernalization) induce VRN1 expression and promote the transition of the apical meristem to the reproductive phase. In contrast to its Arabidopsis homolog (APETALA1), which is mainly expressed in the apical meristem, VRN1 is also expressed at high levels in the leaves, but its function in this tissue is not well understood. Using tetraploid wheat lines with truncation mutations in the two homoeologous copies of VRN1 (henceforth vrn1-null mutants), we demonstrate that a central role of VRN1 in the leaves is to maintain low transcript levels of the VRN2 flowering repressor after vernalization. Transcript levels of VRN2 were gradually down-regulated during vernalization in both mutant and wild-type genotypes, but were up-regulated after vernalization only in the vrn1-null mutants. The up-regulation of VRN2 delayed flowering by repressing the transcription of FT, a flowering-integrator gene that encodes a mobile protein that is transported from the leaves to the apical meristem to induce flowering. The role of VRN2 in the delayed flowering of the vrn1-null mutant was confirmed using double vrn1-vrn2-null mutants, which flowered two months earlier than the vrn1-null mutants. Both mutants produced normal flowers and seeds demonstrating that VRN1 is not essential for wheat flowering, which contradicts current flowering models. This result does not diminish the importance of VRN1 in the seasonal regulation of wheat flowering. The up-regulation of VRN1 during winter is required to maintain low transcript levels of VRN2, accelerate the induction of FT in the leaves, and regulate a timely flowering in the spring. Our results also demonstrate the existence of redundant wheat flowering genes that may provide new targets for engineering wheat varieties better adapted to changing environments.
BackgroundIn cereal crops such as wheat, an optimal timing of developmental transitions is required to maximize grain yield. Many of these developmental changes are precisely regulated by changes in the duration, intensity or quality of light. Phytochromes are dimeric photoreceptors that absorb light maximally in the red and far-red wavelengths and induce large-scale transcriptional changes in response to variation in light quality. In wheat, PHYC is required for early flowering under long days. However, it is currently unknown whether this function requires the presence of PHYB. In this study, we characterized the role of PHYB in wheat development and used RNA-seq to analyze and compare the transcriptomes of phyB-null and phyC-null TILLING mutants.ResultsUnder long-day photoperiods, phyB-null plants exhibit a severe delay in flowering comparable to the delay observed in phyC-null plants. These results demonstrate that both genes are required for the induction of wheat flowering under long days. Using replicated RNA-seq studies we identified 82 genes that are significantly up or down regulated in both the phyB-null and phyC-null mutant relative to their respective wild-type controls. Among these genes are several well-characterized positive regulators of flowering, including PPD1, FT1 and VRN1. Eight-fold more genes were differentially regulated only in the phyB-null mutant (2202) than only in the phyC-null mutant (261). The PHYB-regulated genes were enriched in components of the auxin, gibberellin and brassinosteroid biosynthesis and signaling pathways, and in transcription factors with putative roles in regulating vegetative development and shade-avoidance responses. Several genes involved in abiotic stress tolerance pathways were also found to be regulated by PHYB.ConclusionsPHYB and PHYC are both required for the photoperiodic induction of wheat flowering, whereas PHYB alone regulates a large number of genes involved in hormone biosynthesis and signaling, shade-avoidance response, and abiotic stress tolerance. Our analysis provides a comprehensive overview of the PHYB- and PHYC-mediated transcriptional changes during light signaling, and an initial step towards the dissection of this regulatory gene network in wheat. This further dissection will be required to explore the individual phytochrome-mediated developmental responses and to evaluate their potential to improve wheat adaptation to changing environments.Electronic supplementary materialThe online version of this article (doi:10.1186/s12870-016-0831-3) contains supplementary material, which is available to authorized users.
Wheat vernalization requirement is mainly controlled by the VRN1, VRN2, VRN3, and VRN4 genes. The first three have been cloned and have homoeologs in all three genomes. VRN4 has been found only in the D genome (VRN-D4) and has not been cloned. We constructed a high-density genetic map of the VRN-D4 region and mapped VRN-D4 within a 0.09 cM interval in the centromeric region of chromosome 5D. Using telocentric 5D chromosomes generated from the VRN-D4 donor Triple Dirk F, we determined that VRN-D4 is located on the short arm. The VRN-D4 candidate region is colinear with a 2.24 Mb region on Brachypodium distachyon chromosome 4, which includes 127 predicted genes. Ten of these genes have predicted roles in development but we detected no functional polymorphisms associated to VRN-D4. Two recombination events separated VRN-D4 from TaVIL-D1, the wheat homolog of Arabidopsis vernalization gene VIL1, confirming that this gene is not a candidate for VRN-D4. We detected significant interactions between VRN-D4 and other four genes controlling vernalization requirement (Vrn-A1, Vrn-B1, Vrn-D1, and Vrn-B3), which confirmed that VRN-D4 is part of the vernalization pathway and that it is either upstream or is part of the regulatory feedback loop involving VRN1, VRN2 and VRN3 genes. The precise mapping of VRN-D4 and the characterization of its interactions with other vernalization genes provide valuable information for the utilization of VRN-D4 in wheat improvement and for our current efforts to clone this vernalization gene.Electronic supplementary materialThe online version of this article (doi:10.1007/s00438-013-0788-y) contains supplementary material, which is available to authorized users.
Key message The combination of three non-functional alleles of the flowering repressor VRN2 results in a spring growth habit in wheat. AbstractIn temperate cereals with a winter growth habit, a prolonged exposure to low temperatures (vernalization) accelerates flowering. Before vernalization, the VRN2 locus plays a central role in maintaining flowering repression. Non-functional VRN2 alleles result in spring growth habit and are frequent in diploid wheat and barley. However, in hexaploid wheat, the effect of these non-functional VRN2 alleles is masked by gene redundancy. In this study, we developed a triple VRN2 mutant (synthetic vrn2-null) in hexaploid wheat by combining the non-functional VRN-A2 allele present in most polyploid wheats with a VRN-B2 deletion from tetraploid wheat, and a non-functional VRN-D2 allele from Aegilops tauschii (Ae. tauschii) (the donor of hexaploid wheat D genome). Non-vernalized vrn2-null plants flowered 118 days (P < 2.8E−07) earlier than the winter control, and showed a limited vernalization response. The functional VRN-B2 allele is expressed at higher levels than the functional VRN-D2 allele and showed a stronger repressive effect under partial vernalization (4 °C for 4 weeks), and also in non-vernalized plants carrying only a functional VRN-B2 or VRN-D2 in heterozygous state. These results suggest that different combinations of VRN-B2 and VRN-D2 alleles can be a used to modulate the vernalization response in regions with mild winters. Spring vrn2-null mutants have been selected repeatedly in diploid wheat and barley, suggesting that they may have an adaptative value and that may be useful in hexaploid wheat. Spring wheat breeders can use these new alleles to improve wheat adaptation to different or changing environments.Electronic supplementary materialThe online version of this article (doi:10.1007/s00122-016-2713-3) contains supplementary material, which is available to authorized users.
Flowering time represents an important adaptive trait for temperate cereal crops and may also impact on frost damage in cereal reproductive tissues by enabling escape or by influencing accumulation of genuine tolerance. The Flowering time-2L (Flt-2L) quantitative trait locus (QTL) on the distal end of barley chromosome arm 2HL overlaps with QTL for rachis internode length and reproductive frost damage. Flt-2L was also found to be associated with plant height. By combining marker analysis with phenotyping in progeny families of selected Amagi Nijo x WI2585 F(6) recombinants, we were able to map quantitative flowering time, rachis internode length, and plant height effects on 2HL as discrete Mendelian traits. The three developmental characters showed codominant modes of expression and perfectly cosegregated with one another in a 1.3-cM marker interval, indicating control by the same gene or closely linked genes. Twelve genes were identified in the related intervals in the rice and Brachypodium distachyon genomes. The HvAP2 gene cosegregated with Flt-2L and represents a plausible candidate for Flt-2L, since it is highly similar to the wheat domestication gene Q which has similar developmental effects. These data will contribute to isolation of the Flt-2L gene(s) and help establish the basis of the frost damage QTL.
Frost at flowering can cause significant damage to cereal crops. QTL for low temperature tolerance in reproductive tissues (LTR tolerance) were previously described on barley 2HL and 5HL chromosome arms. With the aim of identifying potential LTR tolerance mechanisms, barley Amagi Nijo x WI2585 and Haruna Nijo x Galleon populations were examined for flowering time and spike morphology traits associated with the LTR tolerance loci. In spring-type progeny of both crosses, winter alleles at the Vrn-H1 vernalization response locus on 5H were linked in coupling with LTR tolerance and were unexpectedly associated with earlier flowering. In contrast, tolerance on 2HL was coupled with late flowering alleles at a locus we named Flt-2L. Both chromosome regions influenced chasmogamy/cleistogamy (open/closed florets), although tolerance was associated with cleistogamy at the 2HL locus and chasmogamy at the 5HL locus. LTR tolerance controlled by both loci was accompanied by shorter spikes, which were due to fewer florets per spike on 5HL, but shorter rachis internodes on 2HL. The Eps-2S locus also segregated in both crosses and influenced spike length and flowering time but not LTR tolerance. Thus, none of the traits was consistently correlated with LTR tolerance, suggesting that the tolerance may be due to some other visible trait or an intrinsic (biochemical) property. Winter alleles at the Vrn-H1 locus and short rachis internodes may be of potential use in barley breeding, as markers for selection of LTR tolerance at 5HL and 2HL loci, respectively.
Ginger (Zingiber officinale Roscoe) is an important horticultural crop, valued for its culinary and medicinal properties. Fusarium yellows of ginger, caused by Fusarium oxysporum f. sp. zingiberi (Foz), is a devastating disease that has significantly reduced the quality and crop yield of ginger worldwide. The compatible interaction between ginger and Foz leading to susceptibility is dissected here. The pathogenicity of two Foz isolates on ginger was confirmed by their ability to colonise ginger and in turn induce both internal and external plant symptoms typical of Fusarium yellows. To shed light on Foz susceptibility at the molecular level, a set of defense-responsive genes was analysed for expression in the roots of ginger cultivars challenged with Foz. These include nucleotide-binding site (NBS) type of resistant (R) genes with a functional role in pathogen recognition, transcription factors associated with systemic acquired resistance, and enzymes involved in terpenoid biosynthesis and cell wall modifications. Among three R genes, the transcripts of ZoNBS1 and ZoNBS3 were rapidly induced by Foz at the onset of infection, and the expression magnitude was cultivar-dependent. These expression characteristics extend to the other genes. This study is the first step in understanding the mechanisms of compatible host–pathogen interactions in ginger.
Exposure of flowering cereal crops to frost can cause sterility and grain damage, resulting in significant losses. However, efforts to breed for improved low temperature tolerance in reproductive tissues (LTR tolerance) has been hampered by the variable nature of natural frost events and the confounding effects of heading time on frost-induced damage in these tissues. Here, we establish conditions for detection of LTR tolerance in barley under reproducible simulated frost conditions in a custom-built frost chamber. An ice nucleator spray was used to minimize potential effects arising from variation in naturally occurring extrinsic nucleation factors. Barley genotypes differing in their field tolerance could be distinguished. Additionally, an LTR tolerance quantitative trait locus (QTL) on the long arm of barley chromosome 2H could be detected in segregating families. In a recombinant family, the QTL was shown to be separable from the effects of the nearby flowering time locus Flt-2L. At a minimum temperature of -3.5 degrees C for 2 h, detection of the LTR tolerance locus was dependent on the presence of the nucleator spray, suggesting that the tolerance relates to freezing rather than chilling, and that it is not the result of plant-encoded variation in ice-nucleating properties of the tiller surface.
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