Worldwide significant amounts of food waste are generated daily causing serious environmental issues, occupying land and requiring expenditure of resources for its treatment. A smart method for handling this food waste problem is the development of novel processes targeting the conversion of this waste into value added products. Although valorization of food waste to biofuels, biochemicals and bio-polymers have been widely investigated, the utilization of food waste streams into biofertiliser has not been intensively reviewed. Conversion of food waste, especially agriculture residues into biofertiliser would reduce its environmental impact, improve nutrition levels of the soil, decrease requirements for synthetic chemical fertiliser and have a direct benefit on food production. This paper reviews recent progress in the field regarding the production of biofertiliser from food waste, using anaerobic digestion, aerobic composting, chemical hydrolysis, in situ degradation and direct burning methods. This review also highlights the latest field applications of biofertiliser derived from various food waste streams. It confirms that the technology for the conversion of food waste to biofertilisers is viable, but the production efficiency could be improved with better process control strategies, strict quality controls, development of a smart product distribution system and adoption of advanced technologies. Field tests have indicated that biofertilisers which are obtained in proper managed AD plants are safe and could partially replace the use of chemical fertilisers in field application.

Development requires the proper execution and regulation of the cell cycle via precise, conserved mechanisms. Critically, the E2F/DP complex controls the expression of essential genes during cell cycle transitions. Here, we discovered the molecular function of the SUMO E3 ligase METHYL METHANESULFONATE SENSITIVITY GENE21 (AtMMS21) in regulating the cell cycle via the E2Fa/DPa pathway. DPa was identified as an AtMMS21-interacting protein and AtMMS21 competes with E2Fa for interaction with DPa. Moreover, DPa is a substrate for SUMOylation mediated by AtMMS21, and this SUMOylation enhances the dissociation of the E2Fa/DPa complex. AtMMS21 also affects the subcellular localization of E2Fa/DPa. The E2Fa/DPa target genes are upregulated in the root of and mutants showed increased endoreplication. Overexpression of affected the root development of , and overexpression of completely recovered the abnormal phenotypes of plants. Our results suggest that AtMMS21 dissociates the E2Fa/DPa complex via competition and SUMOylation in the regulation of plant cell cycle.

Cambogin is a polycyclic polyprenylated acylphoroglucinol (PPAP) from the Garcinia genus, which has been used traditionally for cancer treatment across Southeastern Asia. In this study, we found that cambogin inhibited breast cancer cell proliferation and induced cell apoptosis in vitro. Cambogin induced the activation of the caspase-independent mitochondrial apoptotic pathway, as indicated by an increase in the ratio of Bax/Bcl-2 and the nuclear translocation of apoptosis inducing factor (AIF). Two-dimensional gel electrophoresis and mass spectrometry revealed that the expression of proteins involving in the radical oxygen species (ROS) pathway was among the most affected upon cambogin treatment. Cambogin enhanced cellular ROS production, and induced the activation of the ASK1-MKK4/MKK7-JNK/SAPK signaling pathway. Pretreatment with ROS scavenger N-acetylcysteine (NAC), an antioxidant, or the JNK inhibitor SP600125 was able to restore cell viability in the presence of cambogin. Importantly, cambogin treatment led to the activation of activating transcription factor-2 (ATF-2) and the trimethylation of histone H3K9 in the activator protein 1 (AP-1) binding region of the Bcl-2 gene promoter. Finally, cambogin exhibited a potential antitumor effect in MCF-7 breast cancer xenografts without apparent toxicity. Taken in conjunction, the present study indicates that cambogin can induce breast adenocarcinoma cell apoptosis and therefore represents therapeutic potential for cancer treatment.

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