Modulation of evening complex activity enables north-to-south adaptation of soybean

Soybean,a typical short-day crop,is sensitive to photoperiod,which is a major limiting factor defining its north-to-south cultivation range.The long-juvenile(LJ)trait is controlled primarily by the J locus which has been used for decades by soybean breeders to delay flowering and improve grain yield in tropical regions.The J gene encodes an ortholog of the Arabidopsis Evening Complex(EC)component EARLY FLOWERING 3(ELF3).To identify modifiers of J,we conducted a forward genetic screen and isolated a mutant(eoj57)that in combination with j has longer flowering delay compared with j single mutant plants.Map-based cloning and genome re-sequencing identified eoj57(designated as GmLUX2)as an ortholog of the Arabidopsis EC component LUX ARRHYTHMO(LUX).To validate that GmLUX2 is a modifier of J,we used trans-complementation and identified a natural variant allele with a similar phenotype.We also show that GmLUX2 physically interacts with GmELF3a/b and binds DNA,whereas the mutant and natural variant are attenuated in both activities.Transcriptome analysis shows that the GmLUX2-GmELF3a complex co-regulates the expression of several circadian clock-associated genes and directly represses E1 expression.These results provide mechanistic insight into how GmLUX2-GmELF3 controls flowering time via synergistic regulation of gene expression.These novel insights expand our understanding of the regulation of the EC complex,and facilitate the development of soybean varieties adapted for growth at lower latitudes.

Changing Gly311 to an acidic amino acid in the MATE family protein DTX6 enhances Arabidopsis resistance to the dihydropyridine herbicides

In modern agriculture,frequent application of herbicides may induce the evolution of resistance in plants,but the mechanisms underlying herbicide resistance remain largely unexplored.Here,we report the char-acterization of rtp 1(resistant to paraquat 1),an Arabidopsis mutant showing strong resistance to the widely used herbicides paraquat and diquat.The rtp1 mutant is semi-dominant and carries a point mutation in the gene encoding the multidrug and toxic compound extrusion family protein DTX6,leading to the change of glycine to glutamic acid at residue 311(G311E).The wild-type DTX6 with glycine 311 conferred weak para-quat and diquat resistance when overexpressed,while mutation of glycine 311 to a negatively charged amino acid(G311E or G311D)markedly increased the paraquat and diquat resistance of plants,whereas mutation to a positively charged amino acid(G311R or G311K)compromised the resistance,suggesting that the charge property of residue 311 of DTX6 is critical for the paraquat and diquat resistance of Arabi-dopsis plants.DTX6 is localized in the endomembrane trafficking system and may undergo the endosomal sorting to localize to the vacuole and plasma membrane.Treatment with the V-ATPase inhibitor ConA reduced the paraquat resistance of the rtp1 mutant.Paraquat release and uptake assays demonstrated that DTX6 is involved in both exocytosis and vacuolar sequestration of paraquat.DTX6 and DTX5 show functional redundancy as the dtx5 dtx6 double mutant but not the dtx6 single mutant plants were more sen-sitive to paraquat and diquat than the wild-type plants.Collectively,our work reveals a potential mecha-nism for the evolution of herbicide resistance in weeds and provides a promising gene for the manipulation of plant herbicide resistance.

Mutation of DELAYED GREENING1 impairs chloroplast RNA editing at elevated ambient temperature in Arabidopsis

Chloroplasts are important for plant growth and development.RNA editing in chloroplast converts cytidines(Cs)to uridine s(Us)at specific transcript positions and provides a correction mechanism to restore conserved codons or creates start or stop codons.However,the underlined molecular mechanism is not yet fully unders tood.In the present study,we identi fied a thermo-sensi tive mutantin leaf color 1(tst1)and found that TSL1 is allelic to DELAYED GREENING 1(DG1).The mis sense mutation of DG1 in tsl1 mutant confers a high temperature sensitivity and impaired chloroplast development at an elevated ambient temperature in Arabidopsis.Subsequent analysis showed that chloroplast RNA editing at seve ral sites including accD-2568,ndhD-2,and petL-5 is impaired in tsl1 mutant plants grown at an elevated temperature.DG1 interacts with MORF2 and other proteins such as DYW1 and DYW2 involved in chloroplast RNA editing.In vitro RNA electrophoretic mobility shift assay demonstrated that DG1 binds to RNA targets such as accD,ndhD,and petL.Thus,our results revealed that DG1 is important for maintaining chloroplast mRNA editing in Arabidopsis.

inGAP-family:Accurate Detection of Meiotic Recombination Loci and Causal Mutations by Filtering Out Artificial Variants due to Genome Complexities

Accurately identifying DNA polymorphisms can bridge the gap between phenotypes and genotypes and is essential for molecular marker assisted genetic studies.Genome complexities,including large-scale structural variations,bring great challenges to bioinformatic analysis for obtaining high-confidence genomic variants,as sequence differences between non-allelic loci of two or more genomes can be misinterpreted as polymorphisms.It is important to correctly filter out artificial variants to avoid false genotyping or estimation of allele frequencies.Here,we present an efficient and effective framework,inGAP-family,to discover,filter,and visualize DNA polymorphisms and structural variants(SVs)from alignment of short reads.Applying this method to polymorphism detection on real datasets shows that elimination of artificial variants greatly facilitates the precise identification of meiotic recombination points as well as causal mutations in mutant genomes or quantitative trait loci.In addition,inGAP-family provides a user-friendly graphical interface for detecting polymorphisms and SVs,further evaluating predicted variants and identifying mutations related to genotypes.It is accessible at https://sourceforge.net/projects/ingap-family/.