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During the process of flower opening, most petals move downward in the direction of the pedicel (i.e., epinastic movement). In most Delphinium flowers, however, their two lateral petals display a very peculiar movement, the mirrored helical rotation, which requires the twist of the petal stalk. However, in some lineages, their lateral petals also exhibit asymmetric bending that increases the degree of mirrored helical rotation, facilitating the formation of a 3D final shape. Notably, petal asymmetric bending is a novel trait that has not been noticed yet, so its morphological nature, developmental process, and molecular mechanisms remain largely unknown. Here, by using D. anthriscifolium as a model, we determined that petal asymmetric bending was caused by the localized expansion of cell width, accompanied by the specialized array of cell wall nano-structure, on the adaxial epidermis. Digital gene analyses, gene expression, and functional studies revealed that a class I homeodomain-leucine zipper family transcription factor gene, DeanLATE MERISTEM IDENTITY1 (DeanLMI1), contributes to petal asymmetric bending; knockdown of it led to the formation of explanate 2D petals. Specifically, DeanLMI1 promotes cell expansion in width and influences the arrangement of cell wall nano-structure on the localized adaxial epidermis. These results not only provide a comprehensive portrait of petal asymmetric bending for the first time but also shed some new insights into the mechanisms of flower opening and helical movement in plants. [Display omitted] • A marginal, wedge-shaped fold responds for petal asymmetric bending • The fold is due to greater expansion of cell width on localized adaxial epidermis • The fold is also associated with the specialized array of cell wall nano-structure • A class I HD-Zip gene, DeanLMI1 , plays important roles in petal asymmetric bending During the flower opening of the Delphinium , the pair of lateral petals (if present) display a peculiar movement, the mirrored helical rotation. Zhang et al. discover that an evolutionary novelty, petal asymmetric bending, further reinforces such movement. Using D. anthriscifolium as a model, they provide a comprehensive portrait of this trait. [ABSTRACT FROM AUTHOR]

Summary Cyclin-dependent kinase 9 (CDK9) promotes transcriptional elongation through RNAPII pause release. We now report that CDK9 is also essential for maintaining gene silencing at heterochromatic loci. Through a live cell drug screen with genetic confirmation, we discovered that CDK9 inhibition reactivates epigenetically silenced genes in cancer, leading to restored tumor suppressor gene expression, cell differentiation, and activation of endogenous retrovirus genes. CDK9 inhibition dephosphorylates the SWI/SNF protein BRG1, which contributes to gene reactivation. By optimization through gene expression, we developed a highly selective CDK9 inhibitor (MC180295, IC50 = 5 nM) that has broad anti-cancer activity in vitro and is effective in in vivo cancer models. Additionally, CDK9 inhibition sensitizes to the immune checkpoint inhibitor α-PD-1 in vivo , making it an excellent target for epigenetic therapy of cancer. Graphical Abstract Highlights • CDK9 inhibition reactivates epigenetically silenced genes in multiple cancer cells • CDK9 binds to and phosphorylates BRG1, which contributes to gene silencing • We developed a novel potent and selective CDK9 inhibitor, MC180295 • MC180295 shows promising anti-tumoral and immunosensitization activity Inhibition of a kinase typically associated with transcription elongation complexes leads to reactivation of tumor suppressor genes and increases sensitivity to immunotherapy in cancer models. [ABSTRACT FROM AUTHOR]