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Roses are one of the most important cut flowers among ornamental plants. Rose flower longevity is largely dependent on the timing of petal shedding occurrence. To understand the molecular mechanism underlying petal abscission in rose, we performed transcriptome profiling of the petal abscission zone during petal shedding using Illumina technology. We identified a total of 2592 differentially transcribed genes (DTGs) during rose petal shedding. Gene ontology term enrichment and pathway analysis revealed that major biochemical pathways the DTGs were involved in included ethylene biosynthesis, starch degradation, superpathway of cytosolic glycolysis, pyruvate dehydrogenase and TCA cycle, photorespiration and the lactose degradation III pathway. This suggests that alterations in carbon metabolism are an important part of rose petal abscission. Among these DTGs, approximately 150 genes putatively encoding transcription factors were identified in rose abscission zone. These included zinc finger, WRKY, ERF, and Aux/IAA gene families, suggesting that petal abscission involves complex transcriptional reprogramming. Approximately 108 DTGs were related to hormone pathways, of which auxin and ethylene related DTGs were the largest groups including 52 and 41 genes, respectively. These also included 12 DTGs related to gibberellin and 6 DTGs in jasmonic acid pathway. Surprisingly, no DTGs involved in the biosynthesis/signaling of abscisic acid, cytokinin, brassinosteroid, and salicylic acid pathways were detected. Moreover, among DTGs related to auxin, we identified an Aux/IAA gene RhIAA16 that was up-regulated in response to petal shedding. Down-regulation of RhIAA16 by virus-induced gene silencing in rose promoted petal abscission, suggesting that RhIAA16 plays an important role in rose petal abscission.

Summary: The timing of plant organ abscission is modulated by the balance of two hormones, ethylene and auxin, while the mechanism of organ shedding depends on the loss of middle lamella pectin in the abscission zone (AZ). However, the mechanisms involved in sensing the balance of auxin and ethylene and that affect pectin degradation during abscission are not well understood. In this study, we identified two members of the APETALA2/ethylene‐responsive factor (AP2/ERF) transcription factor family in rose (Rosa hybrida), RhERF1 and RhERF4 which play a role in petal abscission. The expression of RhERF1 and RhERF4 was influenced by ethylene and auxin, respectively. Reduced expression of RhERF1 or RhERF4 was observed to accelerate petal abscission. Global expression analysis and real‐time PCR assays revealed that RhERF1 and RhERF4 modulate the expression of genes encoding pectin‐metabolizing enzymes. A reduction in the abundance of pectin epitopes was detected in the AZs of RhERF1 and RhERF4‐silenced plants by immunofluorescence microscopy analysis. In addition, RhERF1 and RhERF4 were shown to bind to the promoter of the pectin‐metabolizing gene β‐GALACTOSIDASE 1 (RhBGLA1), and reduced expression of RhBGLA1 delayed petal abscission. We conclude that during petal abscission, RhERF1 and RhERF4 integrate and coordinate ethylene and auxin signals to modulate pectin metabolism, in part by regulating the expression of RhBGLA1. Significance Statement: This study reports a mechanism for sensing the auxin/ethylene balance associated with modulating petal abscission via degradation of pectin. We found that the expression levels of RhERF1 and RhERF4 are influenced by ethylene and auxin, respectively, and that RhERF1 and RhERF4 act together to modulate pectin degradation in the abscission zone by directly regulating the β‐galactosidase gene RhBGLA1. [ABSTRACT FROM AUTHOR]

Bacterial blight, caused by Xanthomonas axonopodis pv. dieffenbachiae (Xad) , is the most destructive disease of anthurium worldwide, and no effective control technique has been developed currently. The comprehensive survey and precise detection of the pathogen is essential for evaluating disease progress and strengthening management to avoid a serious epidemic. In this study, a total of 253 blight-suspected samples of anthurum and other Araceae species were collected across the country, and 166 potential pathogenic bacteria strains were isolated and purified, after combined analysis on the characteristics of morphology, pathogenicity, 16S rDNA sequences and amplicons of Aad-specific SCAR markers. Finally, 93 of which were considered as X. axonopodis pv. dieffenbachiae. In addition, by using a nested-PCR in repeated detections, 17 out of 21 prevalent anthurium cultivars without blight symptom exhibited latent infection even in young leaves. The results indicated that the anthurium bacterial blight distributed commonly in growing areas in China, and most of the commercial cultivars had no strong resistance. The identification of Xad infection (latent) would be beneficial for the disease forecasting and management improving in anthurium production. [ABSTRACT FROM AUTHOR]

Material surface micromorphology can modulate cellular behavior and promote osteogenic differentiation through cytoskeletal rearrangement. Bone reconstruction requires precise regulation of gene expression in cells, a process governed by epigenetic mechanisms such as histone modifications, DNA methylation, and chromatin remodeling. We constructed osteon-mimetic concentric microgrooved titanium surfaces with different groove sizes and cultured bone marrow-derived mesenchymal stem cells (BMSCs) on the material surfaces to study how they regulate cell biological behavior and osteogenic differentiation through epigenetics. We found that the cells arranged in concentric circles along the concentric structure in the experimental group, and the concentric microgrooved surface did not inhibit cell proliferation. The results of a series of osteogenic differentiation experiments showed that the concentric microgrooves facilitated calcium deposition and promoted osteogenic differentiation of the BMSCs. Concentric microgrooved titanium surfaces that were 30 μm wide and 10 μm deep promoted osteogenic differentiation of BMSC by increasing WDR5 expression via H3K4 trimethylation upregulation.