Barley lesion mimics, supersusceptible or highly resistant to leaf rust and net blotch

Abstract

Lesion mimic mutants of plants have the feature of spontaneously displaying necrotic spots or bands on their leaves. Lesion mimics have often displayed enhanced resistance to biotrophic pathogens whilst showing increased susceptibility to necrotrophs. This paper identifies three novel, non-allelic mutants of barley (Hordeum vulgare), which spontaneously form necrotic leaf lesions: Necrotic leaf spot 9.3091 (nec9.3091), Mottled leaf 8.1661 (mtt8.1661) and Mottled leaf 9.2721 (mtt9.2721). The Necrotic leaf spot 8.3550 mutant (nec8.3550), formerly known as bst1, was included in the study because it is a lesion mimic mutant belonging to the same original pool. The reactions of the mutants to the biotroph Puccinia hordei and the necrotroph Pyrenophora teres f. sp. teres were investigated. Mutants nec8.3550 and mtt8.1661 were more resistant than the parental Bowman near-isogenic line with the Rph3.c gene (Bowman Rph3.c, NGB 22452) to leaf rust, caused by P. hordei. Mutants nec8.3550, mtt8.1661 and mtt9.2721 were more susceptible than Bowman Rph3.c to net blotch, caused by P. teres f. sp. teres. Autofluorescence was detected in leaf tissues of all mutants. Based on the high expression of the PR1 and Hv-HIR genes, combined with the low susceptibility to P. hordei, nec8.3550 appears to have entered a state of systemic acquired resistance, which is quite distinct from the resistance expressed in mtt8.1661. The latter mutant has low or no expression of PR1 and Hv-HIR genes, yet it is highly resistant to rust. It is also extremely susceptible to net blotch. These mutants can serve as genetic sources of novel disease resistance for barley improvement.

Differential effects of lesion mimic mutants in barley on disease development by facultative pathogens

“…Programmed cell death is critical for many plant developmental processes and defence responses ( Jones, 2001 ). Cell death is typically a component of the defence response against biotrophic pathogens, whereas its role in interactions between plants and facultative pathogens with hemibiotrophic or necrotrophic lifestyles can be somewhat ambivalent ( Jarosch et al , 1999 ; Kumar et al , 2001 ; Mengiste, 2012 ; Saville et al , 2012 ; Wright et al , 2013 ). This investigation, using a collection of diverse lesion mimic mutants that differentially regulate disease symptom expression caused by facultative fungi on barley, highlights the complex relationship between host cell death and disease development in plants.…”

“…Lesion mimic mutants have been extensively studied in relation to plant defence responses and typically show enhanced resistance against biotrophic pathogens such as rusts and mildews ( Kamlofski et al , 2007 ; Zhang et al , 2009 ). More variable responses have been reported between lesion mimics and facultative fungi, ranging from enhanced resistance ( Persson et al , 2008 ; 2009 ) to super-susceptibility ( Wright et al , 2013 ).…”

Association of lesion mimic trait with spot blotch resistance in wheat

“…The positive correlation between LMG and AUDPC was similar to the result reported by Kumar et al (2001) in barley mutants with rapid cell death were more susceptible to spot blotch. Wright et al (2013) also reported that lesion mimic has often displayed enhance resistance to biotrophic pathogen while showing increased susceptibility to necrotroph. A number of lm mutants has been identified and characterized, in barley (Lundqvist et al 1997;Rostoks et al 2003Rostoks et al , 2006.…”

“…Since the survival of a hemibiotrophic pathogen in its necrotrophic phase depends on host cell death as a prerequisite for successful pathogenesis, breakdown of cell survival mechanisms as a result of mutations in the Mlo gene may antagonize plant defence to B. sorokiniana (Kumar et al 2002). Lesion mimic is beneficial if the host is under attack of the biotrophs that need living cells for their infection (Wright et al 2013). Contrary to this, necrotrophs need dead cells for their rapid colonization and inoculum production (Govrin et al 2006).…”