BackgroundAbsence of or low sensitivity to photoperiod is necessary for short-day crops, such as rice and soybean, to adapt to high latitudes. Photoperiod insensitivity in soybeans is controlled by two genetic systems and involves three important maturity genes: E1, a repressor for two soybean orthologs of Arabidopsis FLOWERING LOCUS T (GmFT2a and GmFT5a), and E3 and E4, which are phytochrome A genes. To elucidate the diverse mechanisms underlying photoperiod insensitivity in soybean, we assessed the genotypes of four maturity genes (E1 through E4) in early-flowering photoperiod-insensitive cultivars and their association with post-flowering responses.ResultsWe found two novel dysfunctional alleles in accessions originally considered to have a dominant E3 allele according to known DNA markers. The E3 locus, together with E1 and E4, contained multiple dysfunctional alleles. We identified 15 multi-locus genotypes, which we subdivided into 6 genotypic groups by classifying their alleles by function. Of these, the e1-as/e3/E4 genotypic group required an additional novel gene (different from E1, E3, and E4) to condition photoperiod insensitivity. Despite their common pre-flowering photoperiod insensitivity, accessions with different multi-locus genotypes responded differently to the post-flowering photoperiod. Cultivars carrying E3 or E4 were sensitive to photoperiod for post-flowering characteristics, such as reproductive period and stem growth after flowering. The phytochrome A–regulated expression of the determinate growth habit gene Dt1, an ortholog of Arabidopsis TERMINAL FLOWER1, was involved in the persistence of the vegetative activity at the stem apical meristem of flower-induced plants under long-day conditions.ConclusionsDiverse genetic mechanisms underlie photoperiod insensitivity in soybean. At least three multi-locus genotypes consisting of various allelic combinations at E1, E3, and E4 conferred pre-flowering photoperiod insensitivity to soybean cultivars but led to different responses to photoperiod during post-flowering vegetative and reproductive development. The phyA genes E3 and E4 are major controllers underlying not only pre-flowering but also post-flowering photoperiod responses. The current findings improve our understanding of genetic diversity in pre-flowering photoperiod insensitivity and mechanisms of post-flowering photoperiod responses in soybean.

Many ion channel genes have been associated with human genetic pain disorders. Here we report two large Chinese families with autosomal-dominant episodic pain. We performed a genome-wide linkage scan with microsatellite markers after excluding mutations in three known genes (SCN9A, SCN10A, and TRPA1) that cause similar pain syndrome to our findings, and we mapped the genetic locus to a 7.81 Mb region on chromosome 3p22.3-p21.32. By using whole-exome sequencing followed by conventional Sanger sequencing, we identified two missense mutations in the gene encoding voltage-gated sodium channel Nav1.9 (SCN11A): c.673C>T (p.Arg225Cys) and c.2423C>G (p.Ala808Gly) (one in each family). Each mutation showed a perfect cosegregation with the pain phenotype in the corresponding family, and neither of them was detected in 1,021 normal individuals. Both missense mutations were predicted to change a highly conserved amino acid residue of the human Nav1.9 channel. We expressed the two SCN11A mutants in mouse dorsal root ganglion (DRG) neurons and showed that both mutations enhanced the channel's electrical activities and induced hyperexcitablity of DRG neurons. Taken together, our results suggest that gain-of-function mutations in SCN11A can be causative of an autosomal-dominant episodic pain disorder.

BackgroundUnderstanding the molecular mechanisms of flowering and maturity is important for improving the adaptability and yield of seed crops in different environments. In soybean, a facultative short-day plant, genetic variation at four maturity genes, E1 to E4, plays an important role in adaptation to environments with different photoperiods. However, the molecular basis of natural variation in time to flowering and maturity is poorly understood. Using a cross between early-maturing soybean cultivars, we performed a genetic and molecular study of flowering genes. The progeny of this cross segregated for two maturity loci, E1 and E9. The latter locus was subjected to detailed molecular analysis to identify the responsible gene.ResultsFine mapping, sequencing, and expression analysis revealed that E9 is FT2a, an ortholog of Arabidopsis FLOWERING LOCUS T. Regardless of daylength conditions, the e9 allele was transcribed at a very low level in comparison with the E9 allele and delayed flowering. Despite identical coding sequences, a number of single nucleotide polymorphisms and insertions/deletions were detected in the promoter, untranslated regions, and introns between the two cultivars. Furthermore, the e9 allele had a Ty1/copia–like retrotransposon, SORE-1, inserted in the first intron. Comparison of the expression levels of different alleles among near-isogenic lines and photoperiod-insensitive cultivars indicated that the SORE-1 insertion attenuated FT2a expression by its allele-specific transcriptional repression. SORE-1 was highly methylated, and did not appear to disrupt FT2a RNA processing.ConclusionsThe soybean maturity gene E9 is FT2a, and its recessive allele delays flowering because of lower transcript abundance that is caused by allele-specific transcriptional repression due to the insertion of SORE-1. The FT2a transcript abundance is thus directly associated with the variation in flowering time in soybean. The e9 allele may maintain vegetative growth in early-flowering genetic backgrounds, and also be useful as a long-juvenile allele, which causes late flowering under short-daylength conditions, in low-latitude regions.Electronic supplementary materialThe online version of this article (doi:10.1186/s12870-016-0704-9) contains supplementary material, which is available to authorized users.

Photoperiodism is a rhythmic change of sensitivity to light, which helps plants to adjust flowering time according to seasonal changes in daylength and to adapt to growing conditions at various latitudes. To reveal the molecular basis of photoperiodism in soybean (Glycine max), a facultative short-day plant, we analyzed the transcriptional profiles of the maturity gene E1 family and two FLOWERING LOCUS T (FT) orthologs (FT2a and FT5a). E1, a repressor for FT2a and FT5a, and its two homologs, E1-like-a (E1La) and E1Lb, exhibited two peaks of expression in long days. Using two different approaches (experiments with transition between light and dark phases and night-break experiments), we revealed that the E1 family genes were expressed only during light periods and that their induction after dawn in long days required a period of light before dusk the previous day. In the cultivar Toyomusume, which lacks the E1 gene, virus-induced silencing of E1La and E1Lb up-regulated the expression of FT2a and FT5a and led to early flowering. Therefore, E1, E1La, and E1Lb function similarly in flowering. Regulation of E1 and E1L expression by light was under the control of E3 and E4, which encode phytochrome A proteins. Our data suggest that phytochrome A-mediated transcriptional induction of E1 and its homologs by light plays a critical role in photoperiodic induction of flowering in soybean.