A high virulence and pathotype diversity of Puccinia striiformis f.sp. tritici at its centre of diversity, the Himalayan region of Pakistan
Sajid Ali & Marc Leconte & Hidayatur Rahman &
Muhammad Shahab Saqib & Pierre Gladieux &
Jérôme Enjalbert & Claude de Vallavieille-Pope
Accepted: 11 June 2014 # Koninklijke Nederlandse Planteziektenkundige Vereniging 2014
Abstract Information on the pathogen virulence profile and diversity across locations is crucial for host germplasm improvement and deployment. The rapid acquisition of virulence to host resistance by the wheat yellow/stripe rust pathogen (Puccinia striiformis f.sp. tritici: PST), makes it crucial to know about its virulence and pathotype diversity. Recent studies have shown the plausible centre of origin of the pathogen in the
Himalayan region, with Pakistan being the most ancestral to all other worldwide populations. To assess the status of virulence and pathotype diversity in the
Himalayan region of Pakistan, a set of 127 PST infected wheat samples from eight locations were collected, multiplied and pathotyped using a set of 36 differential lines from the world set, European and Chinese sets, and 9 Avocet Yr isolines. Virulence (Vr) was recorded to 18 out of 24 tested yellow rust resistance (Yr) genes, while a total of 53 pathotypes were detected out of 127 isolates tested. Virulence was found to the resistance genes rarely deployed in Pakistan (Vr8) or even worldwide level (Vr5), while virulence to Vilmorin 23 (Yr3+) was absent in Pakistan, which is common in Europe.
None of the pathotypes was dominant across all locations, however, no clear spatial structuring was observed for the studied locations. Our results suggested a high virulence and pathotype diversity in line with the
Eur J Plant Pathol
Author contributions SA, HR and MSS carried out field assessment and yellow rust sampling. SA, ML and CP did the spore multiplication and pathotyping. SA, PG, CP and JE prepared the manuscript. SA, JE, and CP conceived and designed the study.
All authors read and approved the manuscript.
S. Ali :M. Leconte :C. de Vallavieille-Pope
INRA UR 1290 BIOGER-CPP, BP01, 78850 Thiverval-Grignon, France
S. Ali (*)
Institute of Biotechnology and Genetic Engineering, the University of Agriculture, Peshawar, Pakistan e-mail: firstname.lastname@example.org
Department of Agroecology, Aarhus University, Flakkebjerg,
DK-4200 Slagelse, Denmark
H. Rahman :M. S. Saqib
Department of Plant Breeding and Genetics, the University of
Agriculture, Peshawar, Pakistan
UMR 8079 Ecologie Systematique Evolution, Université
Paris-Sud, CNRS-F, 91405 Orsay, France
Department of Plant and Microbial Biology, University of
California, Berkeley, CA 94720-3102, USA
INRA UMR 320 Génétique Végétale, Ferme du Moulon, 91190 Gif sur Yvette, France previously proposed potential role of sexual recombination in the temporal maintenance of PST in the
Himalayan region of Pakistan. This information should be useful in host resistance gene improvement and deployment.
Keywords Multilocations .Major resistance gene .
Stripe rust .Wheat (Triticum aestivum)
Puccinia striiformis f.sp. tritici (PST) is an airborne biotrophic pathogen, causing the stripe/yellow rust of wheat (Triticum aestivum), a disease of immense economic importance worldwide (Singh et al., 2004;
Chen, 2005; Ali et al., 2009a; Hovmøller et al., 2010). The pathogen flourishes well in mild climate (de Vallavieille-Pope et al., 1995; Hau and de
Vallavieille-Pope, 2006; Mboup et al., 2012) and is thus prevalent in most wheat growing regions (Hovmøller et al., 2011; Ali et al., 2014a). In Pakistan, the northern half of the country is characterized by a mild climate, wi th mild temperatures and high humidi ty predominating from the jointing to grain filling stage of wheat crop growth (Ali et al., 2009b). This makes the area prone to wheat yellow rust epidemics and the disease remains a major threat to wheat production in
Pakistan (Ali et al., 2009c; Hovmøller et al., 2010;
Chaves et al., 2013). Severe epidemics have been caused by this pathogen in Pakistan in recent past causing economic losses (Saari and Prescott, 1985; Kisana et al., 2003; Singh et al., 2004; Bahri et al., 2011). High yields could only be achieved through avoiding losses caused by PST through disease management (de
Vallavieille-Pope et al., 2012; Hawkesford et al., 2013).
Different disease management practices could be used for wheat yellow rust control, including fungicides and genetic resistance. However, exploitation of genetic resistance remains the most efficient yellow rust control method (Pathan and Park, 2007; Ali et al., 2009a; de
Vallavieille-Pope et al., 2012; Paillard et al., 2012).
Development of varieties resistant to the disease is always an important objective in wheat breeding programs for crop improvement (Singh et al., 2004), even some are particularly aimed at resistant variety development (Dedryver et al., 2009; Paillard et al., 2012). At least 53 yellow rust resistance genes have been identified (McIntosh et al., 2010) and several of these have been deployed at different geographical scales (region, country, and continent), resulting in short-term yellow rust control (Stubbs, 1985; Hovmøller, 2001; de
Vallavieille-Pope et al., 2012). These resistance genes, however, became ineffective due to the acquisition of virulence to that particular resistance gene rendering the variety susceptible (Hovmøller, 2001; de VallavieillePope et al., 2012).
The acquisition of virulence by the pathogen is a result of the large scale deployment of a resistant variety, which results in a strong selective pressure on the pathogen population (Johnson, 1992; Line, 2002;McDonald and Linde, 2002). Such a selective pressure against the avirulent types results in a rapid selection of virulent types leading to resistance gene inefficacy and in the subsequent reduction in cultivation of that particular variety (McDonald and Linde, 2002; de VallavieillePope et al., 2012). However, the extent of the response to this selective pressure is directly influenced by the diversity in virulence existing in the pathogen population and its maintenance through different modes of reproduction, which determines its adaptation capacity to host resistance genes (Giraud et al., 2006;