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Both quantitative and qualitative food losses of extremely variable magnitude occur during all harvest and postharvest stages, from harvesting, through handling, storage, processing and marketing, to final delivery to the consumer. The latest values published indicated that industrialized and developing countries dispose of roughly similar quantities of food. Whereas in developed countries the losses occur at the retailer and consumer stages, in the developing countries the losses occur during the production, harvest, postharvest and processing phases, because of poor infrastructure, low levels of technology, and low investment in food production systems. Quality cannot be improved after harvest, only maintained; therefore it is important to harvest fruits, vegetables and flowers at the proper stage and size and at peak quality. Preharvest production practices and factors such as cultivation practices, water supply, type of soil, environmental temperature and mechanical damage may seriously affect postharvest quality and result in the rejection or downgrading of produce at the point of sale. In addition, after harvest, improper temperature and humidity management as well as packaging and handling may have adverse effects on storage life and quality. Thus, integration of treatment methods calls for specific differential combinations of treatments for each product in each country.

Calcium/calmodulin-dependent protein kinase (CaMK), a key downstream target protein in the Ca2+ signaling pathway of eukaryotes, plays an important regulatory role in the growth, development and pathogenicity of plant fungi. Three AaCaMKs (AaCaMK1, AaCaMK2 and AaCaMK3) with conserved PKC_like superfamily domains, ATP binding sites and ACT sites have been cloned from Alternaria alternata, However, their regulatory mechanism in A. alternata remains unclear. In this study, the function of the AaCaMKs in the development, infection structure differentiation and pathogenicity of A. alternata was elucidated through targeted gene disruption. The single disruption of AaCaMKs had no impact on the vegetative growth and spore morphology but significantly influenced hyphae growth, sporulation, biomass accumulation and melanin biosynthesis. Further expression analysis revealed that the AaCaMKs were up-regulated during the infection structure differentiation of A. alternata on hydrophobic and pear wax substrates. In vitro and in vivo analysis further revealed that the deletion of a single AaCaMKs gene significantly reduced the A. alternata conidial germination, appressorium formation and infection hyphae formation. In addition, pharmacological analysis confirmed that the CaMK specific inhibitor, KN93, inhibited conidial germination and appressorium formation in A. alternata. Meanwhile, the AaCaMKs genes deficiency significantly reduced the A. alternata pathogenicity. These results demonstrate that AaCaMKs regulate the development, infection structure differentiation and pathogenicity of A. alternata and provide potential targets for new effective fungicides.

Pathogenic fungi have developed complex and specific infection strategies to invade host tissues successfully. Regulator of G‐protein signalling (RGS) proteins exhibit GTPase‐accelerating protein activities and play a crucial role in the formation of infection structures in pathogenic fungi. However, specific regulatory mechanisms remain unclear. In the present study, observations of infection structure indicated that the deletion of AaRgs2 resulted in a significant increase in spore germination. Appressorium‐like formation rate was compared to that of the wild‐type strain on a Gelbond hydrophobic membrane coated with 16‐hydroxyhexadecanoic acid or 1,16‐hexadecanediol, which are cutin monomers in pear peel. Transcriptome analysis during the appressorium‐like formation stage revealed 4124 differentially expressed genes (DEGs) that were annotated in the wild‐type strain and the ΔAaRgs2 mutant. KEGG enrichment analysis showed that the cAMP‐PKA signalling pathway, MAPK signalling pathway, peroxisome and autophagy pathway were closely associated with appressorium‐like formation regulated by AaRgs2. Yeast two‐hybrid and bimolecular fluorescence complementation assays demonstrated a specific physical interaction between AaRgs2 and AaGα1, further confirming that AaGα1 interacted with the Pfam domain of adenylate cyclase AC. Our studies provide evidence suggesting that AaRgs2 negatively regulates appressorium‐like formation of A. alternata induced by pear cutin monomer via the AaRgs2‐AaGα1‐AaAC module. AaRgs2 negatively regulates appressorium‐like formation of A. alternata induced by pear cutin monomer via the AaRgs2‐AaGα1‐AaAC module.

The fungus Colletotrichum gloeosporioides breaches the fruit cuticle but remains quiescent until fruit ripening signals a switch to necrotrophy, culminating in devastating anthracnose disease. There is a need to understand the distinct fungal arms strategy and the simultaneous fruit response. Transcriptome analysis of fungal–fruit interactions was carried out concurrently in the appressoria, quiescent and necrotrophic stages. Conidia germinating on unripe fruit cuticle showed stage‐specific transcription that was accompanied by massive fruit defense responses. The subsequent quiescent stage showed the development of dendritic‐like structures and swollen hyphae within the fruit epidermis. The quiescent fungal transcriptome was characterized by activation of chromatin remodeling genes and unsuspected environmental alkalization. Fruit response was portrayed by continued highly integrated massive up‐regulation of defense genes. During cuticle infection of green or ripe fruit, fungi recapitulate the same developmental stages but with differing quiescent time spans. The necrotrophic stage showed a dramatic shift in fungal metabolism and up‐regulation of pathogenicity factors. Fruit response to necrotrophy showed activation of the salicylic acid pathway, climaxing in cell death. Transcriptome analysis of C. gloeosporioides infection of fruit reveals its distinct stage‐specific lifestyle and the concurrent changing fruit response, deepening our perception of the unfolding fungal–fruit arms and defenses race.

Background Wound healing is a representative phenomenon of potato tubers subjected to mechanical injuries. Our previous results found that benzo-(1,2,3)-thiadiazole-7-carbothioic acid S-methyl ester (BTH) promoted the wound healing of potato tubers. However, the molecular mechanism related to inducible wound healing remains unknown. Results Transcriptomic evaluation of healing tissues from potato tubers at three stages, namely, 0 d (nonhealing), 5 d (wounded tubers healed for 5 d) and 5 d (BTH-treated tubers healed for 5 d) using RNA-Seq and differentially expressed genes (DEGs) analysis showed that more than 515 million high-quality reads were generated and a total of 7665 DEGs were enriched, and 16 of these DEGs were selected by qRT-PCR analysis to further confirm the RNA sequencing data. Gene ontology (GO) enrichment analysis indicated that the most highly DEGs were involved in metabolic and cellular processes, and KEGG enrichment analysis indicated that a large number of DEGs were associated with plant hormones, starch and sugar metabolism, fatty acid metabolism, phenylpropanoid biosynthesis and terpenoid skeleton biosynthesis. Furthermore, a few candidate transcription factors, including MYB, NAC and WRKY, and genes related to Ca 2+ -mediated signal transduction were also found to be differentially expressed during wound healing. Most of these enriched DEGs were upregulated after BTH treatment. Conclusion This comparative expression profile provided useful resources for studies of the molecular mechanism via these promising candidates involved in natural or elicitor-induced wound healing in potato tubers.

While the details on the mode of action of F-RALF remain to be elucidated, it was recently shown that endogenous RALF-FERONIA signaling leads to inactivation of the plasma membrane H+-ATPase AHA2 and inhibition of plant cell elongation [27]. [...]FERONIA integrates signals from other plant hormones, such as auxin and abscisic acid [28]. Interestingly, the Pma2 clade is present in many phytopathogenic ascomycetes and absent in nonpathogenic species. [...]the acquisition of a second plasma membrane H+-ATPase, in addition to Pma1, with a specific role in virulence, appears to represent a common strategy of ascomycete pathogens. [...]research is also needed to elucidate the pH-sensing processes that link extracellular alkalinization to known pathogenicity signaling modules, such as the Pal/Rim pathway or the IG MAPK cascade. Besides the plasma membrane protein PalH, whose precise mode of pH sensing remains to be defined, additional pH sensors must exist. [...]the recent finding that different antifungals induce a dramatic decrease of pHi in Candida [46, 47], combined with the broadly conserved role of alkalinization in virulence, makes alkalinization an attractive target for the control of fungal pathogens.

Ca2+, as a second messenger in cells, enables organisms to adapt to different environmental stresses by rapidly sensing and responding to external stimuli. In recent years, the Ca2+ mediated calcium signaling pathway has been studied systematically in various mammals and fungi, indicating that the pathway is conserved among organisms. The pathway consists mainly of complex Ca2+ channel proteins, calcium pumps, Ca2+ transporters and many related proteins. Crz1, a transcription factor downstream of the calcium signaling pathway, participates in regulating cell survival, ion homeostasis, infection structure development, cell wall integrity and virulence. This review briefly summarizes the Ca2+ mediated calcium signaling pathway and regulatory roles in plant pathogenic fungi. Based on discussing the structure and localization of transcription factor Crz1, we focus on the regulatory role of Crz1 on growth and development, stress response, pathogenicity of pathogenic fungi and its regulatory mechanisms. Furthermore, we explore the cross-talk between Crz1 and other signaling pathways. Combined with the important role and pathogenic mechanism of Crz1 in fungi, the new strategies in which Crz1 may be used as a target to explore disease control in practice are also discussed.

Aspergillus carbonarius is the major producer of ochratoxin A (OTA) among Aspergillus species, but the contribution of this secondary metabolite to fungal virulence has not been assessed. We characterized the functions and addressed the roles of three factors in the regulation of OTA synthesis and pathogenicity in A. carbonarius: LaeA, a transcriptional factor regulating the production of secondary metabolites; polyketide synthase, required for OTA biosynthesis; and glucose oxidase (GOX), regulating gluconic acid (GLA) accumulation and acidification of the host tissue during fungal growth. Deletion of laeA in A. carbonarius resulted in significantly reduced OTA production in colonized nectarines and grapes. The ∆laeA mutant was unable to efficiently acidify the colonized tissue, as a direct result of diminished GLA production, leading to attenuated virulence in infected fruit compared to the wild type (WT). The designed Acpks‐knockout mutant resulted in complete inhibition of OTA production in vitro and in colonized fruit. Interestingly, physiological analysis revealed that the colonization pattern of the ∆Acpks mutant was similar to that of the WT strain, with high production of GLA in the colonized tissue, suggesting that OTA accumulation does not contribute to A. carbonarius pathogenicity. Disruption of the Acgox gene inactivated GLA production in A. carbonarius, and this mutant showed attenuated virulence in infected fruit compared to the WT strain. These data identify the global regulator LaeA and GOX as critical factors modulating A. carbonarius pathogenicity by controlling transcription of genes important for fungal secondary metabolism and infection. LaeA and GOX are critical factors modulating A. carbonarius pathogenicity in fruits by controlling transcription of genes important for fungal secondary metabolism and infection; OTA does not contribute to A. carbonarius virulence.

Mechanical wound on fruit triggers the formation of reactive oxygen species (ROS) that weaken cell walls, resulting in post-harvest losses. This mechanism can be controlled by using fruit preservatives to stimulate fruit antioxidant enzyme activities for the detoxification of ROS. Chitosan is a safe and environmentally friendly preservative that modulates ROS in whole fruits and plant cells, but the effects of chitosan on the ROS metabolism of mechanically wounded apples during storage are unknown. Our study focused on exploring the effects of post-harvest chitosan treatment on ROS production, cell membrane integrity, and enzymatic and non-enzymatic antioxidant systems at fruit wounds during storage. Apple fruits (cv. Fuji) were artificially wounded, treated with 2.5% (w/v) chitosan, and stored at room temperature (21–25°C, RH = 81–85%) for 7 days. Non-wounded apples were used as healthy controls. The results showed that chitosan treatment stimulated the activities of NADPH oxidase and superoxide dismutase and increased the formation of superoxide anions and hydrogen peroxide in fruit wounds. However, malondialdehyde, lipoxygenase, and membrane permeability, which are direct biomarkers to evaluate lipid peroxidation and membrane integrity, were significantly decreased in the wounded fruits after chitosan treatment compared to the wounded control fruits. Antioxidant enzymes, such as peroxidase and catalase activities, were induced by chitosan at fruit wounds. In addition, ascorbate-glutathione cycle-related enzymes; ascorbate peroxide, monodehydroascorbate reductase, dehydroascorbate reductase, and glutathione reductase and the content of substrates, mainly ascorbic acid, dehydroascorbate, reduced glutathione, and glutathione, were increased at fruit wounds by chitosan compared to the wounded control fruits. Our results show that wounding stimulated the production of ROS or oxidative stress. However, treatment with chitosan triggered antioxidant systems to scavenge ROS and prevent loss of fruit membrane integrity. Therefore, chitosan promises to be a favorable preservative in inducing tolerance to stress and maintaining fruit quality.

Growth of Colletotrichum gloeosporioides in the presence of cation salts NaCl and KCl inhibited fungal growth and anthracnose symptom of colonization. Previous reports indicate that adaptation of Aspergillus nidulans to salt- and osmotic-stress conditions revealed the role of zinc-finger transcription factors SltA and CrzA in cation homeostasis. Homologs of A. nidulans SltA and CrzA were identified in C. gloeosporioides. The C. gloeosporioides CrzA homolog is a 682-amino acid protein, which contains a C2H2 zinc finger DNA-binding domain that is highly conserved among CrzA proteins from yeast and filamentous fungi. The C. gloeosporioides SltA homolog encodes a 775-amino acid protein with strong similarity to A. nidulans SltA and Trichoderma reesei ACE1, and highest conservation in the three zinc-finger regions with almost no changes compared to ACE1 sequences. Knockout of C. gloeosporioides crzA (ΔcrzA) resulted in a phenotype with inhibited growth, sporulation, germination and appressorium formation, indicating the importance of this calciu006D-activated transcription factor in regulating these morphogenetic processes. In contrast, knockout of C. gloeosporioides sltA (ΔsltA) mainly inhibited appressorium formation. Both mutants had reduced pathogenicity on mango and avocado fruit. Inhibition of the different morphogenetic stages in the ΔcrzA mutant was accompanied by drastic inhibition of chitin synthase A and B and glucan synthase, which was partially restored with Ca2+ supplementation. Inhibition of appressorium formation in ΔsltA mutants was accompanied by downregulation of the MAP kinase pmk1 and carnitine acetyl transferase (cat1), genes involved in appressorium formation and colonization, which was restored by Ca2+ supplementation. Furthermore, exposure of C. gloeosporioides ΔcrzA or ΔsltA mutants to cations such as Na+, K+ and Li+ at concentrations that the wild type C. gloeosporioides is not affected had further adverse morphogenetic effects on C. gloeosporioides which were partially or fully restored by Ca2+. Overall results suggest that both genes modulating alkali cation homeostasis have significant morphogenetic effects that reduce C. gloeosporioides colonization.