Diseases affecting wheat: Septoria nodorum blotch

Abstract

Septoria nodorum blotch (SNB) is an important disease affecting wheat in many of its production areas around the world, and is caused by the ascomycete fungal pathogen Parastagonospora nodorum. Breeding for SNB resistance has been hampered by the polygenic and quantitative nature of the resistance, and the farmers often have to rely on fungicides to control the disease. In recent years, substantial progress has been made in understanding the P. nodorum–wheat pathosystem. Several host-specific interactions between necrotrophic effectors (NEs) and host sensitivity (Snn) genes have been identified and play major roles in SNB seedling resistance. Some of the NEs have been cloned and can be used to screen breeding material at the seedling stage. This chapter provides an overview of the molecular understanding of host–pathogen interactions, progress in understanding the genetics of host resistance and use of molecular markers and effector screening as promising tools in resistance breeding for this challenging disease.

Genetic mapping using a wheat multi-founder population reveals a locus on chromosome 2A controlling resistance to both leaf and glume blotch caused by the necrotrophic fungal pathogen Parastagonospora nodorum

“…In contrast to the established relevance of sensitive NE-Snn interactions to field resistance, correlations between seedling resistances and adult plant resistances are low (Shankar et al 2008). This might be because isolates used in such seedling tests produce different NEs in comparison with the NEs which showed effects in the field (Ruud and Lillemo 2018). For instance, Ruud et al (2017) found that when P. nodorum isolate 201618 which lacks the Tox3 gene was used for seedling testing, correlation between seedling disease scores and field disease scores was less significant than those for Tox3 producing isolates.…”

“…One possible reason for an overall lack of strong correlation is that the P. nodorum isolates used for seedling screens might not be the most representative isolates of the local P. nodorum population in the field. Another possible reason would be that some of the field resistances/ susceptibility could not be fully explained by NE-Snn interactions, as up to now, only four such interactions have been found contributing to field resistances/susceptibility (Friesen et al 2009;Phan et al 2016;Ruud and Lillemo 2018). Other underexplored plant resistant mechanisms may be involved in field SNB resistance.…”

“…It can cause lesions on both wheat leaves and glumes, and can reduce grain yield by 30% (Bhathal et al 2003;Wicki et al 1999). Infected seeds and wheat debris are the primary inoculum sources, with infection favored by warm and humid conditions at later wheat developmental stages, as the asexual pycnidiospores are dispersed by rain-splash (Blixt et al 2008;King et al 1983;Ruud and Lillemo 2018;Sommerhalder et al 2011). Currently, control of SNB relies heavily on fungicide application.…”

“…P. nodorum NEs are small secreted proteins, previously called host-selective toxins (HSTs), which act as virulence factors facilitating disease development (Liu et al 2004a, b). Up to now, eight NEs have been identified which interact with nine wheat sensitivity loci (Ruud and Lillemo 2018;Shi et al 2015). Among those, only three P. nodorum NE genes have been cloned: ToxA, Tox1 and Tox3 (Friesen et al 2009;Liu et al 2009Liu et al , 2012.…”

“…While both leaf blotch and glume blotch are caused by the same pathogen on the same host, the inheritance of resistance to glume blotch is reported to be genetically different from leaf blotch (Chu et al 2010;Wicki et al 1999;Xu et al 2004). Eighteen QTL have previously been identified for glume blotch resistance on chromosomes 2A, 2B, 2D, 3B, 4B, 5A, 6B and 7D, reviewed by Ruud and Lillemo (2018). However, most glume blotch studies were undertaken before Friesen et al (2007) hypothesized the inverse gene-for-gene model for leaf blotch, and the resistance/sensitivity mechanism for glume blotch is still unclear (Solomon et al 2006;Uphaus et al 2007;Wainshilbaum and Lipps 1991;Wicki et al 1999).…”