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Recent investigations have shown that more than one third of harvested fruit and vegetables are lost (FAO, 2011; USDA, 2014; OECD, 2014). Most losses occur due to pathogen infections in the field or after harvest, which lead to postharvest decay, when fruit ripen and vegetables senesce. Moreover, during the last decade, several postharvest fungicides that often had wide spectra of targets have been withdrawn from the market, due to: (i) selection of resistant fungal isolates; (ii) toxicity to humans and the environment; (iii) increasing consumer concern toward risk of pesticide residues on products, with the consequent strict requirements from several major supply chains for the quantity and number of active ingredient(s) on foodstuffs, as percentages of maximum residue limit; and (iv) increasing costs of registration and re-registration (Romanazzi et al., 2016a). Therefore, there is growing interest in finding cheap, safe, and eco-friendly alternatives to synthetic fungicides for the control of postharvest decay * Corresponding author. of fresh produce. Induction of plant resistance by biological, chemical, or physical means is considered a sustainable strategy to manage postharvest decay of fruit and vegetables. This approach has gained increasing interest during recent years, in which we can see a high trend in papers dealing with induced resistance, from few ones recorded 30 years ago to more than 800 recorded yearly in 2013–2015 (Fig. 1), and due to new tools, further knowledge has been obtained on host responses to various methods of control (Hershkovitz et al., 2013; Gapper et al., 2014). The beneficial effects of induced resistance in the postharvest environment were originally demonstrated about two decades ago. For example, the use of heat treatment to decrease chilling injury and disease incidence in fruit through the induction of host resistance has been extensively studied (Lurie and Pedreschi, 2014). Ultraviolet-C (UV-C) irradiation and exposure to sunlight have been shown to induce resistance to pathogens and chilling tolerance in many harvested commodities (Wilson et al., 1994; Ruan et al., 2015; Sivankalyani et al., 2016). More recently, different inducers, such as cell-wall components, plant extracts, compounds of biological origin, and synthetic chemicals, have been shown to trigger plant resistance to pathogen attack locally and systemically (Walters and Fountaine, 2009). Moreover, biological control agents can induce plant resistance to pathogens (Vallad and Goodman, 2004; Da Rocha and Hammerschmidt, 2005; Lyon, 2007). However, to correctly induce resistance in different plants, it is necessary to know and understand the host–microbe interactions, and the effects on postharvest physiology and handling of the different fruit and vegetables (Da Rocha and Hammerschmidt, 2005). Here, we review the different biological, physical, and chemical inducers that have been shown to control postharvest diseases of fruit and vegetables, and highlight their proposed mechanisms of action.
2. Mechanisms involved in induced resistance
Various biotic inducers (e.g., fungi, bacteria, viruses, phytoplasma, insects) and abiotic stresses (e.g., chemical and physical inducers) can trigger resistance in plants, which is known as ‘induced resistance’ (Pieterse et al., 2012; Walters et al., 2013; Pieterse et al., 2014). These can produce rapid expression of defense responses (Conrath et al., 2002; Fu and Dong, 2013). Examples of treatments able to induce resistance in host tissues and of representative mechanisms involved are reported in Fig. 2. We can imagine induced resistance as produced by an array of treatments that elicit a cloud of defense responses. There are two types of induced resistance in plants: systemic acquired resistance (SAR) and induced systemic resistance (ISR). Both of these mechanisms can induce defenses that confer long-lasting protection against a broad spectrum of microorganisms, and are mediated by phytohormones, such as salicylic acid (SA), jasmonic acid (JA), and ethylene (ET). SAR requires the signal molecule SA and is associated with accumulation of pathogenesis-related (PR) proteins, which are believed to contribute to resistance (Durrant and Dong, 2004). Instead, the ISR pathway functions independently of SA, while it is dependent on JA and ET (Van Wees et al., 1999). This induced resistance does not directly activate plant defense responses, but activates the plant to a state of ‘alertness’, so that a future pathogen attack will be strongly and efficiently responded to. This phenomenon is also known as the ‘priming effect’ (Conrath et al., 2006; Jung et al., 2009), and one of the most known priming effects is root colonization by plant-growth-promoting rhizobacteria (PGPR), which induce plant development and ISR-mediated resistance (Vallad and Goodman, 2004; Verhage et al., 2010). While PGPR induces ISR, other inducers can activate SAR or both of these systems.