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Branching is an important agronomic trait that is conducive to plant architecture and yield in flowering Chinese cabbage. Plant branching is regulated by a complex network mediated by hormones; gibberellin (GA) is one of the important hormones which is involved in the formation of shoot branching. Research on the regulatory mechanism of GA influencing rosette branch numbers is limited for flowering Chinese cabbage. In this study, the exogenous application of 600 mg/L GA3 effectively inhibited rosette branching and promoted internode elongation in flowering Chinese cabbage. RNA-Seq analysis further found that these DEGs were significantly enriched in 'the plant hormone signal transduction' pathways, and auxin-related genes were significantly differentially expressed between MB and MB_GA. The upregulation of auxin (AUX) and the upregulation of auxin/indole-3-acetic acid (AUX/IAA), as well as the downregulation of SMALL AUXIN-UPREGULATED RNA (SAUR), were found in the negative regulation of the rosette branching. The qRT-PCR results showed that the expression of AUX/IAA and SAUR from IAA gene family members were consistent with the results of transcriptome data. Phytohormone profiling by targeted metabolism revealed that endogenous auxin contents were significantly increased in MB_GA. Transcriptome and metabolome analysis clarified the main plant hormones and genes underlying the rosette branching in flowering Chinese cabbage, confirming that auxin could inhibit rosette branching. In this regard, the results present a novel angle for revealing the mechanism of gibberellin acting on the branching architecture in flowering Chinese cabbage. [ABSTRACT FROM AUTHOR]

Kaposi's sarcoma-associated herpesvirus (KSHV) can cause a variety of malignancies. Ganciclovir (GCV) is one of the most efficient drugs against KSHV, but its non-specificity can cause other side effects in patients. Nucleic acid miR-34a-5p can inhibit the transcription of KSHV RNA and has great potential in anti-KSHV therapy, but there are still problems such as easy degradation and low delivery efficiency. Here, we constructed a co-loaded dual-drug nanocomplex (GCV@ZIF-8/PEI-FA+miR-34a-5p) that contains GCV internally and adsorbs miR-34a-5p externally. The folic acid (FA)-coupled polyethyleneimine (PEI) coating layer (PEI-FA) was shown to increase the cellular uptake of the nanocomplex, which is conducive to the enrichment of drugs at the KSHV infection site. GCV and miR-34a-5p are released at the site of the KSHV infection through the acid hydrolysis characteristics of ZIF-8 and the "proton sponge effect" of PEI. The co-loaded dual-drug nanocomplex not only inhibits the proliferation and migration of KSHV-positive cells but also decreases the mRNA expression level of KSHV lytic and latent genes. In conclusion, this co-loaded dual-drug nanocomplex may provide an attractive strategy for antiviral drug delivery and anti-KSHV therapy. [ABSTRACT FROM AUTHOR]