The genus Aquilegia (Ranunculaceae) has been cultivated as ornamental and medicinal plants for centuries. With petal spurs of strikingly diverse size and shape, Aquilegia has also been recognized as an excellent system for evolutionary studies. Pollinator‐mediated selection for longer spurs is believed to have shaped the evolution of this genus, especially the North American taxa. Recently, however, an opposite evolutionary trend was reported in an Asian lineage, where multiple origins of mini- or even nonspurred morphs have occurred. Interesting as it is, the lack of genomic resources has limited our ability to decipher the molecular and evolutionary mechanisms underlying spur reduction in this special lineage. Using long-read sequencing (PacBio Sequel), in combination with optical maps (BioNano DLS) and Hi–C, we assembled a high-quality reference genome of A. oxysepala var. kansuensis, a sister species to the nonspurred taxon. The final assembly is approximately 293.2 Mb, 94.6% (277.4 Mb) of which has been anchored to 7 pseudochromosomes. A total of 25,571 protein-coding genes were predicted, with 97.2% being functionally annotated. When comparing this genome with that of A. coerulea, we detected a large rearrangement between Chr1 and Chr4, which might have caused the Chr4 of A. oxysepala var. kansuensis to partly deviate from the “decaying” path that was taken before the split of Aquilegia and Semiaquilegia. This high-quality reference genome is fundamental to further investigations on the development and evolution of petal spurs and provides a strong foundation for the breeding of new horticultural Aquilegia cultivars.

Integrin β1 (ITGB1), which acts as an extracellular matrix (ECM) receptor, has gained increasing attention as a therapeutic target for the treatment of hepatocellular carcinoma (HCC). However, the underpinning mechanism of how ITGB1 drives HCC progression remains elusive. In this study, we first found that ITGB1 expression was significantly higher in HCC tissues than in normal controls by bioinformatics analysis. Furthermore, bioinformatics analysis revealed that paxillin (PXN) and 14-3-3 protein zeta (YWHAZ) are the molecules participating in ITGB1-regulated HCC tumor cell cycle progression. Indeed, immunohistochemistry (IHC) revealed that ITGB1, paxillin, and YWHAZ were strongly upregulated in paired HCC tissue compared with adjacent normal tissues. Notably, the inhibition of ITGB1 expression by small interfering RNA (siRNA) resulted in the downregulated expression of PXN and YWHAZ in primary HCC cells, as assessed by western blot and immunostaining. In addition, ITGB1 knockdown markedly impaired the aggressive behavior of HCC tumor cells and delayed cell cycle progression as determined by cell migration assay, drug-resistance analysis, colony formation assay, quantitative real-time polymerase chain reaction (qRT-PCR), and cell cycle analysis as well as cell viability measurements. More importantly, we proved that xenograft ITGB1high tumors grew more rapidly than ITGB1low tumors. Altogether, our study showed that the ITGB1/PXN/YWHAZ/protein kinase B (AKT) axis enhances HCC progression by accelerating the cell cycle process, which offers a promising approach to halt HCC tumor growth.