Genetic interactions between FLM and other flowering-time genes in Arabidopsis thaliana

FLOWERING LOCUS M (FLM) is a MADS-domain gene that acts as an inhibitor of flowering in Arabidopsis. Here we describe the genetic interaction of FLM with genes in the photoperiod and autonomous flowering pathways. Although the sequence of FLM is most similar to that of FLC, FLM and FLC interact with different flowering pathways. It has been previously shown that flc lesions suppress the late-flowering phenotype of FRI-containing lines and autonomous-pathway mutants. However, flm lesions suppress the late-flowering phenotype of photoperiod-pathway mutants but not that of FRI-containing lines or autonomous-pathway mutants. Another MADS-domain flowering repressor with a mutant phenotype similar to FLM is SVP. The late-flowering phenotype of FLM over-expression is suppressed by the svp mutation, and an svp flm double mutant behaves like the single mutants. Thus FLM and SVP are in the same flowering pathway which interacts with the photoperiod pathway. Abbreviations: CO, CONSTANS; FLC, FLOWERING LOCUS C; FLM, FLOWERING LOCUS M; FRI, FRIGIDA; GI, GIGANTEA; LD, LUMINIDEPENDENS; SVP, SHORT VEGETATIVE PHASE; FCA is not an abbreviation     

拟南芥At1g10300基因调节叶形和开花时间

核仁G蛋白1(Nucleolar G protein 1,NOG1)是一种高度保守的核仁GTP酶,在真核生物中广泛存在,参与60 S核糖体亚基前体的组装。在线虫中敲减NOG1的表达造成生长缓慢、虫体变小和寿命延长的表型,而过量表达NOG1则使线虫的寿命缩短。拟南芥的At1g10300基因注释为NOG1-2,但是其生物学功能还有待研究。该研究对其功能进行了初步研究,首先检测了该基因在拟南芥各个器官的表达情况。结果表明:该基因在7 d龄幼苗、茎生叶和花中均有表达,其中在花中表达量最高。获得了At1g10300基因的T-DNA插入突变体,发现在长日照条件下,At1g10300突变体植株的莲座紧凑,莲座叶片长宽比降低,但叶面积和植株高度与野生型相比无显著差异,表明其叶形发生改变;突变体植株的抽薹时间晚于野生型。荧光定量RT-PCR结果表明,突变体植株中开花促进因子FT、CO和GI的表达水平下调,而开花抑制因子FLC的表达水平上调。以上结果揭示At1g10300基因的突变影响了FT、CO、GI及FLC基因的表达,使植株出现晚花表型。     

The molecular mechanism of vernalization in Arabidopsis and cereals: role of Flowering Locus C and its homologs

Winter varieties of plants can flower only after exposure to prolonged cold. This phenomenon is known as vernalization and has been widely studied in the model plant Arabidopsis thaliana as well as in monocots. Through the repression of floral activator genes, vernalization prevents flowering in winter. In Arabidopsis, FLOWERING LOCUS C or FLC is the key repressor during vernalization, while in monocots vernalization is regulated through VRN1, VRN2 and VRN3 (or FLOWERING LOCUS T). Interestingly, VRN genes are not homologous to FLC but FLC homologs are found to have a significant role in vernalization response in cereals. The presence of FLC homologs in monocots opens new dimensions to understand, compare and retrace the evolution of vernalization pathways between monocots and dicots. In this review, we discuss the molecular mechanism of vernalization-induced flowering along with epigenetic regulations in Arabidopsis and temperate cereals. A better understanding of cold-induced flowering will be helpful in crop breeding strategies to modify the vernalization requirement of economically important temperate cereals.     

FLC: A key regulator of flowering time in Arabidopsis

The timing of floral transition has significant consequences for reproductive success in plants. The molecular genetic dissection of flowering time control in Arabidopsis identified an integrated network of pathways that quantitatively control this developmental switch. A central player in this process is the FLOWERING LOCUS C gene (FLC), which blocks flowering by inhibiting the genes required to switch the meristem from vegetative to floral development. Three systems (the FRIGIDA gene, vernalization, and the autonomous pathway) all influence the state of FLC. Last years many new genes have been identified that regulate FLC expression, and most of them are involved in the modification of FLC chromatin. This review focuses on recent insights in FLC regulation.     

The BAF60 Subunit of the SWI/SNF Chromatin-Remodeling Complex Directly Controls the Formation of a Gene Loop at FLOWERING LOCUS C in Arabidopsis

SWI/SNF complexes mediate ATP-dependent chromatin remodeling to regulate gene expression. Many components of these complexes are evolutionarily conserved, and several subunits of Arabidopsis thaliana SWI/SNF complexes are involved in the control of flowering, a process that depends on the floral repressor FLOWERING LOCUS C (FLC). BAF60 is a SWI/SNF subunit, and in this work, we show that BAF60, via a direct targeting of the floral repressor FLC, induces a change at the high-order chromatin level and represses the photoperiod flowering pathway in Arabidopsis. BAF60 accumulates in the nucleus and controls the formation of the FLC gene loop by modulation of histone density, composition, and posttranslational modification. Physiological analysis of BAF60 RNA interference mutant lines allowed us to propose that this chromatin-remodeling protein creates a repressive chromatin configuration at the FLC locus.     

Brahma is required for proper expression of the floral repressor FLC in Arabidopsis

Background

BRAHMA (BRM) is a member of a family of ATPases of the SWI/SNF chromatin remodeling complexes from Arabidopsis. BRM has been previously shown to be crucial for vegetative and reproductive development.

Methodology/Principal Findings

Here we carry out a detailed analysis of the flowering phenotype of brm mutant plants which reveals that, in addition to repressing the flowering promoting genes CONSTANS (CO), FLOWERING LOCUS T (FT) and SUPPRESSOR OF OVEREXPRESSION OF CO1 (SOC1), BRM also represses expression of the general flowering repressor FLOWERING LOCUS C (FLC). Thus, in brm mutant plants FLC expression is elevated, and FLC chromatin exhibits increased levels of histone H3 lysine 4 tri-methylation and decreased levels of H3 lysine 27 tri-methylation, indicating that BRM imposes a repressive chromatin configuration at the FLC locus. However, brm mutants display a normal vernalization response, indicating that BRM is not involved in vernalization-mediated FLC repression. Analysis of double mutants suggests that BRM is partially redundant with the autonomous pathway. Analysis of genetic interactions between BRM and the histone H2A.Z deposition machinery demonstrates that brm mutations overcome a requirement of H2A.Z for FLC activation suggesting that in the absence of BRM, a constitutively open chromatin conformation renders H2A.Z dispensable.

Conclusions/Significance

BRM is critical for phase transition in Arabidopsis. Thus, BRM represses expression of the flowering promoting genes CO, FT and SOC1 and of the flowering repressor FLC. Our results indicate that BRM controls expression of FLC by creating a repressive chromatin configuration of the locus.     

Growth habit determination by the balance of histone methylation activities in Arabidopsis

In Arabidopsis, the rapid‐flowering summer‐annual versus the vernalization‐requiring winter‐annual growth habit is determined by natural variation in FRIGIDA (FRI) and FLOWERING LOCUS C (FLC). However, the biochemical basis of how FRI confers a winter‐annual habit remains elusive. Here, we show that FRI elevates FLC expression by enhancement of histone methyltransferase (HMT) activity. EARLY FLOWERING IN SHORT DAYS (EFS), which is essential for FRI function, is demonstrated to be a novel dual substrate (histone H3 lysine 4 (H3K4) and H3K36)‐specific HMT. FRI is recruited into FLC chromatin through EFS and in turn enhances EFS activity and engages additional HMTs. At FLC, the HMT activity of EFS is balanced by the H3K4/H3K36‐ and H3K4‐specific histone demethylase (HDM) activities of autonomous‐pathway components, RELATIVE OF EARLY FLOWERING 6 and FLOWERING LOCUS D, respectively. Loss of HDM activity in summer annuals results in dominant HMT activity, leading to conversion to a winter‐annual habit in the absence of FRI. Thus, our study provides a model of how growth habit is determined through the balance of the H3K4/H3K36‐specific HMT and HDM activities.     

Genome‐wide association analyses reveal complex genetic architecture underlying natural variation for flowering time in canola

Optimum flowering time is the key to maximize canola production in order to meet global demand of vegetable oil, biodiesel and canola‐meal. We reveal extensive variation in flowering time across diverse genotypes of canola under field, glasshouse and controlled environmental conditions. We conduct a genome‐wide association study and identify 69 single nucleotide polymorphism (SNP) markers associated with flowering time, which are repeatedly detected across experiments. Several associated SNPs occur in clusters across the canola genome; seven of them were detected within 20 Kb regions of a priori candidate genes; FLOWERING LOCUS T, FRUITFUL, FLOWERING LOCUS C, CONSTANS, FRIGIDA, PHYTOCHROME B and an additional five SNPs were localized within 14 Kb of a previously identified quantitative trait loci for flowering time. Expression analyses showed that among FLC paralogs, BnFLC.A2 accounts for ~23% of natural variation in diverse accessions. Genome‐wide association analysis for FLC expression levels mapped not only BnFLC.C2 but also other loci that contribute to variation in FLC expression. In addition to revealing the complex genetic architecture of flowering time variation, we demonstrate that the identified SNPs can be modelled to predict flowering time in diverse canola germplasm accurately and hence are suitable for genomic selection of adaptative traits in canola improvement programmes.     

Aldehyde dehydrogenase ALDH3F1 involvement in flowering time regulation through histone acetylation modulation on FLOWERING LOCUS C

Flowering time regulation is one of the most important processes in the whole life of flowering plants and FLOWERING LOCUS C (FLC) is a central repressor of flowering time. However, whether metabolic acetate level affects flowering time is unknown. Here we report that ALDEHYDE DEHYDROGENASE ALDH3F1 plays essential roles in floral transition via FLC‐dependent pathway. In the aldh3f1‐1 mutant, the flowering time was significant earlier than Col‐0 and the FLC expression level was reduced. ALDH3F1 had aldehyde dehydrogenase activity to affect the acetate level in plants, and the amino acids of E214 and C252 are essential for its catalytic activity. Moreover, aldh3f1 mutation reduced acetate level and the total acetylation on histone H3. The H3K9Ac level on FLC locus was decreased in aldh3f1‐1, which reduced FLC expression. Expression of ALDH3F1 could rescue the decreased H3K9Ac level on FLC, FLC expression and also the early‐flowering phenotype of aldh3f1‐1, however ALDH3F1^E214A or ALDH3F1^C252A could not. Our findings demonstrate that ALDH3F1 participates in flowering time regulation through modulating the supply of acetate for acetyl‐CoA, which functions as histone acetylation donor to modulate H3K9Ac on FLC locus.