The ancient gymnosperm genus Taxus is the exclusive source of the anticancer drug paclitaxel, yet no reference genome sequences are available for comprehensively elucidating the paclitaxel biosynthesis pathway. We have completed a chromosome-level genome of Taxus chinensis var. mairei with a total length of 10.23 gigabases. Taxus shared an ancestral whole-genome duplication with the coniferophyte lineage and underwent distinct transposon evolution. We discovered a unique physical and functional grouping of CYP725As (cytochrome P450) in the Taxus genome for paclitaxel biosynthesis. We also identified a gene cluster for taxadiene biosynthesis, which was formed mainly by gene duplications. This study will facilitate the elucidation of paclitaxel biosynthesis and unleash the biotechnological potential of Taxus.

Ginkgo has unique reference value for studying sex differences and determination in plants. We identified its sex‐determining region and revealed the metabolic variation resulting from the sex differences. The study provides a novel foundation for understanding Ginkgo sexual dimorphism.

SummaryGenes of the mixed lineage leukemia (MLL) family regulate transcription by methylating histone H3K4. Six members of the MLL family exist in humans, including SETD1A, SETD1B and MLL1-MLL4. Each of them plays non-redundant roles in development and disease genesis. MLL1 regulates the cell cycle and the oscillation of circadian gene expression. Its fusion proteins are involved in leukemogenesis. Here, we studied the role of MLL1 in innate immunity and found it selectively regulates the activation of genes downstream of NF-kB mediated by tumor necrosis factor (TNFa) and lipopolysaccharide (LPS). Real-time PCR and genome-wide gene expression profile analysis proved that the deficiency of MLL1 reduced the expression of a group of genes downstream of nuclear factor kB (NF-kB). However, the activation of NF-kB itself was not affected. The MLL1 complex is found both in the nucleus and cytoplasm and is associated with NF-kB. CHIP assays proved that the translocation of MLL1 to chromatin was dependent on NF-kB. Our results suggest that MLL1 is recruited to its target genes by activated NF-kB and regulates their transcription.