Two interacting basic helix-loop-helix transcription factors control flowering time in rice.

Flowering time is one of the most important agronomic traits affecting the adaptation and yield of rice (Oryza sativa). Heading date 1 (Hd1) is a key factor in the photoperiodic control of flowering time. In this study, two basic helix-loop-helix (bHLH) transcription factors, Hd1 Binding Protein 1 (HBP1) and Partner of HBP1 (POH1) were identified as transcriptional regulators of Hd1. We generated knockout mutants of HBP1 and ectopically expressed transgenic lines of the two bHLH transcription factors and used these lines to investigate the roles of these two factors in regulating flowering time. HBP1 physically associated with POH1 forming homo- or heterodimers to perform their functions. Both HBP1 and POH1 bound directly to the cis-acting elements located in the promoter of Hd1 to activate its expression. CRISPR/Cas9-generated knockout mutations of HBP1, but not POH1 mutations, promoted earlier flowering time; conversely, HBP1 and POH1 overexpression delayed flowering time in rice under long-day and short-day conditions by activating the expression of Hd1 and suppressing the expression of Early heading date 1 (Ehd1), Heading date 3a (Hd3a), and Rice Flowering locus T 1 (RFT1), thus controlling flowering time in rice. Our findings revealed a mechanism for flowering time control through transcriptional regulation of Hd1 and laid theoretical and practical foundations for improving the growth period, adaptation, and yield of rice.

Comparative metabolomic and transcriptomic analysis reveals a coexpression network of the carotenoid metabolism pathway in the panicle of Setaria italica.

BACKGROUND: The grains of foxtail millet are enriched in carotenoids, which endow this plant with a yellow color and extremely high nutritional value. However, the underlying molecular regulation mechanism and gene coexpression network remain unclear. METHODS: The carotenoid species and content were detected by HPLC for two foxtail millet varieties at three panicle development stages. Based on a homologous sequence BLAST analysis, these genes related to carotenoid metabolism were identified from the foxtail millet genome database. The conserved protein domains, chromosome locations, gene structures and phylogenetic trees were analyzed using bioinformatics tools. RNA-seq was performed for these samples to identify differentially expressed genes (DEGs). A Pearson correlation analysis was performed between the expression of genes related to carotenoid metabolism and the content of carotenoid metabolites. Furthermore, the expression levels of the key DEGs were verified by qRT-PCR. The gene coexpression network was constructed by a weighted gene coexpression network analysis (WGCNA). RESULT: The major carotenoid metabolites in the panicles of DHD and JG21 were lutein and ß-carotene. These carotenoid metabolite contents sharply decreased during the panicle development stage. The lutein and ß-carotene contents were highest at the S1 stage of DHD, with values of 11.474 µg /100 mg and 12.524 µg /100 mg, respectively. Fifty-four genes related to carotenoid metabolism were identified in the foxtail millet genome. Cis-acting element analysis showed that these gene promoters mainly contain 'plant hormone', 'drought stress resistance', 'MYB binding site', 'endosperm specific' and 'seed specific' cis-acting elements and especially the 'light-responsive' and 'ABA-responsive' elements. In the carotenoid metabolic pathways, SiHDS, SiHMGS3, SiPDS and SiNCED1 were more highly expressed in the panicle of foxtail millet. The expression of SiCMT, SiAACT3, SiPSY1, SiZEP1/2, and SiCCD8c/8d was significantly correlated with the lutein content. The expression of SiCMT, SiHDR, SiIDI2, SiAACT3, SiPSY1, and SiZEP1/2 was significantly correlated with the content of ß-carotene. WGCNA showed that the coral module was highly correlated with lutein and ß-carotene, and 13 structural genes from the carotenoid biosynthetic pathway were identified. Network visualization revealed 25 intramodular hub genes that putatively control carotenoid metabolism. CONCLUSION: Based on the integrative analysis of the transcriptomics and carotenoid metabonomics, we found that DEGs related to carotenoid metabolism had a stronger correlation with the key carotenoid metabolite content. The correlation analysis and WGCNA identified and predicted the gene regulation network related to carotenoid metabolism. These results lay the foundation for exploring the key target genes regulating carotenoid metabolism flux in the panicle of foxtail millet. We hope that these target genes could be used to genetically modify millet to enhance the carotenoid content in the future.

Correction to: SKIP controls flowering time via the alternative splicing of SEF pre-mRNA in Arabidopsis.

Upon publication of the original article [1], the authors noticed that they omitted Additional file 16: Table S10 from the Additional file list. Additional file 16: Table S10 can be found attached to this Correction and the caption of this Additional file can be found below.

SKIP controls flowering time via the alternative splicing of SEF pre-mRNA in Arabidopsis.

BACKGROUND: Similar to other eukaryotes, splicing is emerging as an important process affecting development and stress tolerance in plants. Ski-interacting protein (SKIP), a splicing factor, is essential for circadian clock function and abiotic stress tolerance; however, the mechanisms whereby it regulates flowering time are unknown. RESULTS: In this study, we found that SKIP is required for the splicing of serrated leaves and early flowering (SEF) pre-messenger RNA (mRNA), which encodes a component of the ATP-dependent SWR1 chromatin remodeling complex (SWR1-C). Defects in the splicing of SEF pre-mRNA reduced H2A.Z enrichment at FLC, MAF4, and MAF5, suppressed the expression of these genes, and produced an early flowering phenotype in skip-1 plants. CONCLUSIONS: Our findings indicate that SKIP regulates SWR1-C function via alternative splicing to control the floral transition in Arabidopsis thaliana.