During their evolution plants have developed several inducible mechanisms against pathogen attack. A first infection can trigger systemic resistance reactions that render the plant less susceptible to the pathogens. This phenomenon, if persist over the time can involve the whole plant and is defined as SAR (Systemic Acquired Resistance) activation (Durrat e Dong, 2004). Some non-pathogenic rhizobacteria can also reduce disease through the stimulation of inducible plant defence mechanisms that render the host more resistant to further pathogens ingress, a phenomenon termed induced systemic resistance (ISR) (Ongena and Jacques, 2007). Recent investigation showed that bacterial strains belonging to Bacillus species are able to both directly suppress the pathogen infections and stimulate the host defences. In these mechanisms of action some bacterial biomolecules, belonging to lipopeptides family (surfactins, iturins and fengycins) can play a key role as repressive and/or stimulator factors. In particular, these compounds can be involved in rhizosphere competence (biofilm formation and spreader), in direct inhibition of phytopathogens (antagonism) and host plant immunization (Ongena et al., 2007). Moreover lipopeptides can also act sinergically (Maget-Dana R. et al., 1992; Ongena et al., 2007; Romero et al., 2007). Recently, our researches were aimed to study the effect of selected antagonist bacteria and their purified and characterized bioactive molecules on both plant and pathogen. Preliminary results showed as some antagonist bacteria and their active biomolecules were able to inhibit in vitro different fungal pathogens as well as to reduce the severity of symptoms caused by Fusarium oxysporum f.sp. lycopersici on tomato and by Podosphaera xanthii on zucchini plants. Investigations are also in progress to elucidate the putative induced resistance mechanisms involved in the interaction antagonist-host-pathogen.

Antagonist activity of selected bacteria and their biomolecules against fungal pathogen and possible induction of resistance in horticultural plants

LIMA, Giuseppe;DE CURTIS, Filippo;
2009-01-01

Abstract

During their evolution plants have developed several inducible mechanisms against pathogen attack. A first infection can trigger systemic resistance reactions that render the plant less susceptible to the pathogens. This phenomenon, if persist over the time can involve the whole plant and is defined as SAR (Systemic Acquired Resistance) activation (Durrat e Dong, 2004). Some non-pathogenic rhizobacteria can also reduce disease through the stimulation of inducible plant defence mechanisms that render the host more resistant to further pathogens ingress, a phenomenon termed induced systemic resistance (ISR) (Ongena and Jacques, 2007). Recent investigation showed that bacterial strains belonging to Bacillus species are able to both directly suppress the pathogen infections and stimulate the host defences. In these mechanisms of action some bacterial biomolecules, belonging to lipopeptides family (surfactins, iturins and fengycins) can play a key role as repressive and/or stimulator factors. In particular, these compounds can be involved in rhizosphere competence (biofilm formation and spreader), in direct inhibition of phytopathogens (antagonism) and host plant immunization (Ongena et al., 2007). Moreover lipopeptides can also act sinergically (Maget-Dana R. et al., 1992; Ongena et al., 2007; Romero et al., 2007). Recently, our researches were aimed to study the effect of selected antagonist bacteria and their purified and characterized bioactive molecules on both plant and pathogen. Preliminary results showed as some antagonist bacteria and their active biomolecules were able to inhibit in vitro different fungal pathogens as well as to reduce the severity of symptoms caused by Fusarium oxysporum f.sp. lycopersici on tomato and by Podosphaera xanthii on zucchini plants. Investigations are also in progress to elucidate the putative induced resistance mechanisms involved in the interaction antagonist-host-pathogen.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11695/8465
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