Background Patulin is a mycotoxin made by the causal agent of blue mildew of stored pome fruits, and many other types of filamentous fungi. genes had been those involved with transportation and oxidation-reduction procedures, recommending the activation of body’s defence mechanism to resist patulin toxicity and expel the mycotoxin from the cells. Various other upregulated genes encoded protein involved with metabolic procedures such as for example those of the thioredoxin and glutathione systems, which are crucial to revive the mobile redox homeostasis. Conversely, patulin treatment reduced the appearance of genes mixed up in procedures of proteins adjustment and synthesis, AV-951 such as for example transcription, RNA digesting, translation, proteins biosynthesis and phosphorylation of proteins. Also, genes encoding protein involved in transportation of ions, cell division and cell cycle were downregulated. This indicates a reduction of metabolic activity, probably due to the high energy requirement from the cells or metabolic arrest while recovering from the insult caused by patulin toxicity. Conclusions Complex mechanisms are triggered inside a biocontrol candida in response to patulin. The genes recognized in this study can pave the way to develop i) a biodetoxification process of patulin in juices and ii) a biosensor for the quick and cost-effective detection of this mycotoxin. Electronic supplementary material The online version of this article (doi:10.1186/s12864-016-2550-4) contains supplementary material, which is available to authorized users. and on cells exposed to PAT exposed increased levels of transcripts of genes involved in proteasome activity, rate of metabolism of sulfur Ly6c amino acids, and stress reactions, which included transporters involved in detoxification and multidrug resistance, oxidative stress scavengers (thioredoxin and glutathione) and DNA restoration genes . Another study in the fission candida confirmed the ROS-induced PAT toxicity through glutathione (GSH) depletion, and the activation of antioxidants and redox systems controlled from the transcription element Pap1 , which is the ortholog of Yap1, a key transcription element that mediates oxidative stress reactions in [11, 12] and . Moreover, in PAT also causes plasma membrane fluidization  and changes in chromatin structure . In mammals, the primary target organs of PAT toxicity are the gastrointestinal tract, kidney, liver and the immune system, with acute symptoms of intestinal hemorrhage, ulceration, nausea, edema, dyspnea, convulsion, and agitation. The carcinogenic risk of PAT is definitely classified in group 3 from the International Agency for Study on Cancer , since the evidence for its carcinogenicity is considered inadequate in humans and experimental animals. Long-term consequences of exposure to toxic PAT concentrations may AV-951 include mutagenicity, genotoxicity, embryotoxicity, and exposure to high dosages may include immunosuppression, immunotoxicity and neurotoxicity [1, 2, 17]. The Joint Food and Agriculture Organization/World Health Organization Expert Committee on Food Additives established a maximum tolerable daily intake for PAT of 0.4?mg/kg body weight/day . Based upon its toxicity profile, legislative regulations in Europe and USA set the highest tolerable levels of PAT in fruit-based products and juices at 50?g/kg, and for baby food at 10?g/kg (EC Regulation 1881/2006). Not surprisingly restrictive legislation, latest surveys in USA and Europe revealed that PAT contamination continues to be a common problem [19C21]. Furthermore to undesireable effects on mammals, PAT inhibits AV-951 microbial development, having antibacterial, antifungal and antiviral activities, and problems vegetable cells . Much like additional secondary metabolites made by filamentous fungi, the part of PAT will probably assist in competition against additional microbes that those fungi encounter within their environment. A gene cluster encoding proteins for PAT biosynthesis continues to be determined [2, 22], and mutation of the genes allowed the analysis of the part of PAT in the pathogenicity which is still questionable and likely reliant on sponsor elements [23C26]. Postharvest control of attacks is crucial to avoid PAT build up in.