Inheritance of maize resistance to gibberella and fusarium ear rots and kernel contamination with deoxynivalenol and fumonisinsby A. Butrón, L. M. Reid, R. Santiago, A. Cao, R. A. Malvar

Plant Pathology


Agronomy and Crop Science / Horticulture / Plant Science / Genetics


Maize Kernel Antioxidants and Their Potential Involvement in Fusarium Ear Rot Resistance

Adeline Picot, Vessela Atanasova-Pénichon, Sebastien Pons, Gisèle Marchegay, Christian Barreau, Laëtitia Pinson-Gadais, Joël Roucolle, Florie Daveau, Daniel Caron, Florence Richard-Forget

QTL mapping of resistance to Fusarium ear rot using a RIL population in maize

Jun-Qiang Ding, Xiao-Ming Wang, Subhash Chander, Jian-Bing Yan, Jian-Sheng Li


Inheritance of maize resistance to gibberella and fusarium ear rots and kernel contamination with deoxynivalenol and fumonisins

A. Butrona*, L. M. Reidb, R. Santiagoa†, A. Caoa† and R. A. Malvara aMision Biologica de Galicia (CSIC), Apdo. 28, 36080, Pontevedra, Spain; and bEastern Cereal and Oilseed Research Centre, Central

Experimental Farm, Agriculture and Agri-Food Canada, Ottawa, ON K1A 0C6, Canada

The objective of this study was to investigate the stability, across well-differentiated environments, of genetic control of maize resistance to Fusarium graminearum and Fusarium verticillioides ear rots and mycotoxin contamination, found in genotypes of diverse origin and adapted to different environments. This knowledge will help to design the most appropriate breeding programme to reduce mycotoxin content across a wide range of environments. Although maize genetics involved in resistance to ear rots and mycotoxin contamination greatly depended on the environment, additive and dominance effects were the predominant genetic effects in most environments. The stability across environments for resistance to ear rots and deoxynivalenol and fumonisin contamination was low, and recommended target areas of breeding programmes for either Fusarium species are different based on the different nature of genetic effect 9 environment interactions for each species. In general, the classification of inbreds and hybrids according to their resistance levels was similar across environments, suggesting that the same sources of resistance could be suitable for different environments, and breeding for resistance to one species would affect resistance to the other one.

Keywords: ear rot, generation-mean analyses, genetic effects, maize, mycotoxin, Zea mays


Fusarium graminearum and Fusarium verticillioides are the most common fungal pathogens associated with maize (Zea mays) in temperate regions. These fungi cause ear rots known as gibberella and fusarium ear rot (GER and FER), respectively, and contaminate maize kernels with mycotoxins. Deoxynivalenol (DON) is the most important mycotoxin produced by F. graminearum;

DON causes vomiting and diarrhoea, immunosuppression, and is responsible for the feed refusal syndrome of livestock (Pestka, 2007). Fusarium verticillioides produces fumonisins (FBs) that cause leukoencephalomalacia in horses, pulmonary oedema in pigs, reduced growth in poultry and hepatic and immune disorders in cattle (Voss et al., 2007); the International Agency for Research on

Cancer has classified the fumonisin toxins as probably carcinogenic (IARC, 2002). Therefore, legislation to limit the amount of these mycotoxins has been implemented in many parts of the world.

The distribution and occurrence of GER and FER are related to geographical and climatic conditions: in general, wetter and cooler conditions are more favourable for GER while drier and warmer conditions favour FER. In Ontario, Canada, maize kernels are frequently contaminated with both F. graminearum and

F. verticillioides, and consequently with DON and FBs (Hooker & Schaafsma, 2005). However, in northwestern Spain, F. verticillioides is the most prevalent fungus (Aguın et al., 2014), but appreciable levels of DON can also be present due to F. graminearum (Butron et al., 2006).

Kernel detoxification and the application of cultural practices to reduce mycotoxin levels are not always feasible; however, plant breeding is emerging as an effective and environmentally safe method to control Fusarium infection and reduce mycotoxin levels in susceptible crops (Eller et al., 2008). The improvement of maize with higher resistance to kernel mycotoxin contamination is highly feasible considering the moderate-to-high heritabilities for DON and FB content (Robertson et al., 2006; L€offler et al., 2011); however, direct selection for mycotoxin contamination is expensive and time-consuming (Eller et al., 2010). Resistance to ear rot could be a cheaper and less time-consuming selection criterion for performing indirect selection because high correlations between GER and FER with DON and FB content, respectively, have been reported (Eller et al., 2010;

L€offler et al., 2011; Martin et al., 2012b), although heritability for ear rot resistance was lower than that for mycotoxin content (Robertson et al., 2006). *E-mail: †Present address: Agrobiologıa Ambiental, Calidad de Suelos y

Plantas (UVIGO), Unidad Asociada a la Mision Biologica de

Galicia (CSIC), Universidad de Vigo, Facultad de Biologıa,

Dpto. Biologıa Vegetal y Ciencias del Suelo, Campus As Lagoas

Marcosende, 36310, Vigo, Spain ª 2015 British Society for Plant Pathology 1

Plant Pathology (2015) Doi: 10.1111/ppa.12351

The genetic architecture of resistance to GER and

FER, and DON and FB contamination, appear complex with many quantitative trait loci (QTLs) of small effects controlling each trait. Some QTLs have possible pleiotropic effects on both ear rot resistance traits and mycotoxin accumulation, and some QTLs for GER and FER resistance are clustered (Perez Brito et al., 2001; Ali et al., 2005; Ding et al., 2008; Xiang et al., 2010; Martin et al., 2011, 2012b). Although additive effects have been reported as being most important for the inheritance of resistance to GER and DON accumulation, dominance as well as epistatic effects could also play a role in the inheritance of these traits (Reid et al., 1994, 2009; Chungu et al., 1996; L€offler et al., 2011; Martin et al., 2011, 2012a). Similar results were reported for the genetics of resistance to FER and FB accumulation (Nankam & Pataky, 1996; Perez Brito et al., 2001; Clements et al., 2004; Robertson-Hoyt et al., 2006; Reid et al., 2009; Williams & Windham, 2009; Hung & Holland, 2012).

Genotypic stability of resistance to ear rot and mycotoxin contamination across different environments has been reported even when genotype evaluations were done in a wide range of environments (Presello et al., 2006; Robertson et al., 2006; Hung & Holland, 2012);