BackgroundFlower development is central to angiosperm reproduction and is regulated by a broad range of endogenous and exogenous stimuli. It has been well documented that ambient temperature plays a key role in controlling flowering time; however, the mechanisms by which temperature regulates floral organ differentiation remain largely unknown.ResultsIn this study, we show that low temperature treatment significantly increases petal number in rose (Rosa hybrida) through the promotion of stamen petaloidy. Quantitative RT-PCR analysis revealed that the expression pattern of RhAG, a rose homolog of the Arabidopsis thaliana AGAMOUS C-function gene, is associated with low temperature regulated flower development. Silencing of RhAG mimicked the impact of low temperature treatments on petal development by significantly increasing petal number through an increased production of petaloid stamens. In situ hybridization studies further revealed that low temperature restricts its spatial expression area. Analysis of DNA methylation level showed that low temperature treatment enhances the methylation level of the RhAG promoter, and a specific promoter region that was hypermethylated at CHH loci under low temperature conditions, was identified by bisulfite sequencing. This suggests that epigenetic DNA methylation contributes to the ambient temperature modulation of RhAG expression.DiscussionOur results provide highlights in the role of RhAG gene in petal number determination and add a new layer of complexity in the regulation of floral organ development.ConclusionsWe propose that RhAG plays an essential role in rose flower patterning by regulating petal development, and that low temperatures increase petal number, at least in part, by suppressing RhAG expression via enhancing DNA CHH hypermethylation of the RhAG promoter.Electronic supplementary materialThe online version of this article (doi:10.1186/s12870-015-0623-1) contains supplementary material, which is available to authorized users.

Rose (Rosa hybrida) plants are major ornamental species worldwide, and their commercial value greatly depends on their open flowers, as both the quality of fully open petals and long vase life are important. Petal senescence can be started and accelerated by various hormone signals, and ethylene is considered an accelerator of petal senescence in rose. To date, however, the underlying mechanism of signaling crosstalk between ethylene and other hormones such as JA in petal senescence remains largely unknown. Here, we isolated RhMYB108, an R2R3-MYB transcription factor, which is highly expressed in senescing petals as well as in petals treated with exogenous ethylene and JA. Applications of exogenous ethylene and JA markedly accelerated petal senescence, while the process was delayed in response to applications of 1-MCP, an ethylene action inhibitor. In addition, silencing of RhMYB108 alter the expression of SAGs such as RhNAC029, RhNAC053, RhNAC092, RhSAG12, and RhSAG113, and finally block ethylene-and JA-induced petal senescence. Furthermore, RhMYB108 was identified to target the promoters of RhNAC053, RhNAC092, and RhSAG113. Our results reveal a model in which RhMYB108 functions as a receptor of ethylene and JA signals to modulate the onset of petal senescence by targeting and enhancing senescence-associated gene expression.

Dichlorvos (O,O-dimethyl O-(2,2-dichlorovinyl)phosphate, DDVP) is a widely acknowledged broad-spectrum organophosphorus insecticide and acaracide. This pesticide has been used for more than four decades and is still in strong demand in many developing countries. Extensive application of DDVP in agriculture has caused severe hazardous impacts on living systems. The International Agency for Research on Cancer of the World Health Organization considered DDVP among the list of 2B carcinogens, which means a certain extent of cancer risk. Hence, removing DDVP from the environment has attracted worldwide attention. Many studies have tested the removal of DDVP using different kinds of physicochemical methods including gas phase surface discharge plasma, physical adsorption, hydrodynamic cavitation, and nanoparticles. Compared to physicochemical methods, microbial degradation is regarded as an environmentally friendly approach to solve several environmental issues caused by pesticides. Till now, several DDVP-degrading microbes have been isolated and reported, including but not limited to Cunninghamella, Fusarium, Talaromyces, Aspergillus, Penicillium, Ochrobium, Pseudomonas, Bacillus, and Trichoderma. Moreover, the possible degradation pathways of DDVP and the transformation of several metabolites have been fully explored. In addition, there are a few studies on DDVP-degrading enzymes and the corresponding genes in microorganisms. However, further research relevant to molecular biology and genetics are still needed to explore the bioremediation of DDVP. This review summarizes the latest development in DDVP degradation and provides reasonable and scientific advice for pesticide removal in contaminated environments.

Rose plants are one of the most important horticultural crops, whose commercial value mainly depends on long-distance transportation, and wounding and ethylene are the main factors leading to their quality decline and accelerated senescence in the process. However, underlying molecular mechanisms of crosstalk between wounding and ethylene in the regulation of flower senescence remain poorly understood. In relation to this, transcriptome analysis was performed on rose flowers subjected to various treatments, including control, wounding, ethylene, and wounding- and ethylene- (EW) dual treatment. A large number of differentially expressed genes (DEGs) were identified, ranging from 2,442 between the ethylene- and control-treated groups to 4,055 between the EW- and control-treated groups. Using weighted gene co-expression network analysis (WGCNA), we identified a hub gene RhWRKY33 (rchiobhmchr5g0071811), accumulated in the nucleus, where it may function as a transcription factor. Moreover, quantitative reverse transcription PCR (RT-qPCR) results showed that the expression of RhWRKY33 was higher in the wounding-, ethylene, and EW-treated petals than in the control-treated petals. We also functionally characterized the RhWRKY33 gene through virus-induced gene silencing (VIGS). The silencing of RhWRKY33 significantly delayed the senescence process in the different treatments (control, wounding, ethylene, and EW). Meanwhile, we found that the effect of RhWRKY33-silenced petals under ethylene and EW dual-treatment were stronger than those under wounding treatment in delaying the petal senescence process, implying that RhWRKY33 is closely involved with ethylene and wounding mediated petal senescence. Overall, the results indicate that RhWRKY33 positively regulates the onset of floral senescence mediated by both ethylene and wounding signaling, but relies heavily on ethylene signaling.

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