Project description:Salicylic acid (SA) is an important plant hormone that regulates defense responses and leaf senescence. It is imperative to understand upstream factors that regulate genes of SA biosynthesis. SAG202/SARD1 is a key regulator for isochorismate synthase 1 (ICS1) induction and SA biosynthesis in defense responses. The regulatory mechanism of SA biosynthesis during leaf senescence is not well understood. Here we show that AtNAP, a senescence-specific NAC family transcription factor, directly regulates a senescence-associated gene named SAG202 as revealed in yeast one-hybrid and in planta assays. Inducible overexpreesion of AtNAP and SAG202 lead to high levels of SA and precocious senescence in leaves. Individual knockout mutants of sag202 and ics1 have markedly reduced SA levels and display a significantly delayed leaf senescence phenotype. Furthermore, SA positively feedback regulates AtNAP and SAG202. Our research has uncovered a unique positive feedback regulatory loop, SA-AtNAP-SAG202-ICS1-SA, that operates to control SA biosynthesis associated with leaf senescence but not defense response.
Project description:This experiment contains a subset of data from the BLUEPRINT Epigenome project ( http://www.blueprint-epigenome.eu ), which aims at producing a reference haemopoetic epigenomes for the research community. 29 samples of primary cells or cultured primary cells of different haemopoeitc lineages from cord blood are included in this experiment. This ArrayExpress record contains only meta-data. Raw data files have been archived at the European Genome-Phenome Archive (EGA, www.ebi.ac.uk/ega) by the consortium, with restricted access to protect sample donors' identity. The relevant accessions of EGA data sets is EGAD00001001165. Details on how to apply for data access via the BLUEPRINT data access committee are on the EGA data set pages. The mapping of samples to these EGA accessions can be found in the 'Sample Data Relationship Format' file of this ArrayExpress record. Information on individual samples and sequencing libraries can also be found on the BLUEPRINT data coordination centre (DCC) website: http://dcc.blueprint-epigenome.eu
Project description:This experiment contains a subset of data from the BLUEPRINT Epigenome project ( http://www.blueprint-epigenome.eu ), which aims at producing a reference haemopoetic epigenomes for the research community. 4 samples of primary cells from tonsil with cell surface markes CD20med/CD38high in young individuals (3 to 10 years old) are included in this experiment. This ArrayExpress record contains only meta-data. Raw data files have been archived at the European Genome-Phenome Archive (EGA, www.ebi.ac.uk/ega) by the consortium, with restricted access to protect sample donors' identity. The relevant accessions of EGA data sets is EGAD00001001523. Details on how to apply for data access via the BLUEPRINT data access committee are on the EGA data set pages. The mapping of samples to these EGA accessions can be found in the 'Sample Data Relationship Format' file of this ArrayExpress record. Information on individual samples and sequencing libraries can also be found on the BLUEPRINT data coordination centre (DCC) website: http://dcc.blueprint-epigenome.eu
Project description:Reprogramming of histone modification regulates gene expression and mammal preimplantation development. Trimethylation of lysine 4 on histone 3 (H3K4me3) has unique landscape in mouse oocytes and early embryos. However, the dynamics and function of H3K4me3 in livestock embryos remain unclear. To address how it is reprogrammed in domestic animals, we profiled changes of H3K4me3 during bovine early embryo development. Notably, the overall signal of H3K4me3 decreased during embryonic genome activation (EGA). By utilizing ultra-low-input native ChIP-seq (ULI-NChIP-seq) technology, we observed widespread broad H3K4me3 domains in oocytes and embryos. The signal of broad H3K4me3 began to decrease after fertilization and was lowest after EGA. Along with the removal of broad H3K4me3, deposition of H3K4me3 at promoter regions enhanced gradually. Besides, the transcriptional activity and signal of promoter H3K4me3 showed positive correlation after the erasure of broad H3K4me3 at 16-cell stage. Moreover, knocking down of demethylases KDM5A, KDM5B and KDM5C caused EGA delay and blastocyst formation failure. RNA-seq analysis revealed 47.8% down-regulated genes in knockdown embryos at 8/16-cell stage were EGA genes, and 63.1% of up-regulated genes were maternal transcripts. Particularly, the positive correlation between transcriptional activity and promoter H3K4me3 during EGA was restrained when knocking down of KDM5A, KDM5B and KDM5C. Overall, our work initiatively mapped the genomic reprogramming of H3K4me3 during bovine preimplantation development, and KDM5A/B/C played roles in modulating oocyte-to-embryonic transition (OET) through timely erasure of broad H3K4me3 domains far away from promoters.
Project description:Reprogramming of histone modification regulates gene expression and mammal preimplantation development. Trimethylation of lysine 4 on histone 3 (H3K4me3) has unique landscape in mouse oocytes and early embryos. However, the dynamics and function of H3K4me3 in livestock embryos remain unclear. To address how it is reprogrammed in domestic animals, we profiled changes of H3K4me3 during bovine early embryo development. Notably, the overall signal of H3K4me3 decreased during embryonic genome activation (EGA). By utilizing ultra-low-input native ChIP-seq (ULI-NChIP-seq) technology, we observed widespread broad H3K4me3 domains in oocytes and embryos. The signal of broad H3K4me3 began to decrease after fertilization and was lowest after EGA. Along with the removal of broad H3K4me3, deposition of H3K4me3 at promoter regions enhanced gradually. Besides, the transcriptional activity and signal of promoter H3K4me3 showed positive correlation after the erasure of broad H3K4me3 at 16-cell stage. Moreover, knocking down of demethylases KDM5A, KDM5B and KDM5C caused EGA delay and blastocyst formation failure. RNA-seq analysis revealed 47.8% down-regulated genes in knockdown embryos at 8/16-cell stage were EGA genes, and 63.1% of up-regulated genes were maternal transcripts. Particularly, the positive correlation between transcriptional activity and promoter H3K4me3 during EGA was restrained when knocking down of KDM5A, KDM5B and KDM5C. Overall, our work initiatively mapped the genomic reprogramming of H3K4me3 during bovine preimplantation development, and KDM5A/B/C played roles in modulating oocyte-to-embryonic transition (OET) through timely erasure of broad H3K4me3 domains far away from promoters.