Population changes in Phytophthora infestans in Taiwan associated with the appearance of resistance to metalaxyl

Abstract

In recent years, late blight, caused by Phytophthora infestans (Mont) De Bary, has increased in severity in many parts of the world, and this has been associated with migrations which have introduced new, arguably more aggressive, populations of the pathogen. In Taiwan, late blight has been endemic on outdoor tomato crops grown in the highlands since the early 1900s, but recent epidemics have been more damaging. To ascertain the present status of the Taiwanese population of P infestans, 139 isolates of the pathogen collected and maintained by the Asian Vegetable Research and Development Center (AVRDC) were characterized using mating type, metalaxyl sensitivity, allozyme genotype, mitochondrial haplotype and RFLP fingerprinting. Up to 1997, all isolates were found to belong to the old clonal lineage of P infestans (US-1 and variants), but in isolates from 1998 a new genotype appeared, and by 2000 this had apparently completely displaced the old population. This new genotype was an A1 mating type and has the dilocus allozyme genotype 100/100/111, 100/100 for the loci coding for glucose-6-phosphate isomerase and peptidase, respectively. These characters, together with RG57 fingerprinting, indicated that these isolates belonged to the US-11 clonal lineage, a minority (11%) being a previously unreported variant of US-11. Whereas metalaxyl-resistant isolates were not detected in the old population, 96% of the new genotypes proved resistant, with the remainder being intermediate in sensitivity. It may be inferred from this sudden, marked change in the characteristics of the Taiwanese P infestans that a new population of the pathogen was introduced around 1997-98 and that this may well have already been metalaxyl-resistant when it arrived, although a role for in situ selection cannot be excluded.

Phenotypic and Genotypic Characterization of Phytophthora infestans Isolates from China

“…All isolates characterized can be ascribed to the ‘new’ population on the basis of resistance to metalaxyl, IIa and IIb mtDNA haplotypes, and allozyme alleles including 100 for Pep and 86, 100, or 111 for Gpi . These results are consistent with a replacement of ‘old’ genotype (US‐1) by ‘new’ migrant one (US‐11) in Taiwan populations of P. infestans (Deahl et al., 2002). Due to the lack of isolates collection before 1998, however, we do not know when the replacement started and how rapidly the shifts have taken place in China.…”

“…Since the early 1980s, dramatic changes have been repeatedly reported for P. infestans populations including uneven mating type distribution, a rapidly increasing, but now stabilized proportion of isolates demonstrating resistance to phenylamide fungicides (Shattock et al., 1990; Gisi and Cohen, 1996; Gotoh et al., 2005), and the substitution of ‘old’ by ‘new’ genotypes (Spielman et al., 1991; Drenth et al., 1994; Deahl et al., 2002). The shifts in population structures were mainly based on differences between ‘old’ (mtDNA haplotype Ib) and ‘new’ (mtDNA haplotype IIb) isolates on Gpi and Pep alleles and RFLP fingerprinting with probe RG57 (Spielman et al., 1991; Deahl et al., 2002), as well as genotype diversity and race composition (Lebreton et al., 1998). mtDNA haplotyping differentiates among only four genotypes.…”

“…The genotypic and phenotypic diversity of P. infestans populations has been investigated in many countries (Fry et al., 1991; Lebreton et al., 1998; Deahl et al., 2002; Cooke et al., 2003; Day et al., 2004; Gotoh et al., 2005). Many reports indicated that new populations of P. infestans appear as a result of migration into regions and/or sexual (asexual) recombination within them (Knapova and Gisi, 2002; Cooke et al., 2003; Gotoh et al., 2005).…”

“…Analyses of allozyme markers and DNA fingerprints of isolates from a number of locations around the world supported the notion that the aforementioned changes resulted from the displacement of an ‘old’ world‐wide clonal lineage (US‐1) by a new population of P. infestans (Spielman et al., 1991; Drenth et al., 1994). The old population consisted exclusively of the mating type A1, mtDNA haplotype Ib, allozyme genotypes glucose‐6‐phosphate isomerase ( Gpi )86/100 and peptidase ( Pep )92/100, and characteristic RG57 fingerprint isolates, whereas the new population contained isolates of both the A1 and A2 mating types, IIa and IIb mtDNA haplotypes, Gpi 100/100/111 and Pep 100/100 (Spielman et al., 1991; Day and Shattock, 1997; Lebreton et al., 1998; Deahl et al., 2002). A concomitant increase in the complexity of virulent phenotypes and tolerance to the specific fungicide metalaxyl was observed worldwide (Fry et al., 1991).…”

Characterization of Phytophthora infestans Isolates from Jersey, Channel Islands

“…Although only just over a quarter of potato crops from which isolates were obtained had been phenylamide-treated, all of the isolates from potato were metalaxyl-resistant. The absence of metalaxyl-sensitive isolates among the P. infestans genotypes from potato suggests that in Jersey, metalaxyl resistance may have originated from ingress of already metalaxyl-resistant strains, as is believed to have occurred in the USA (Goodwin et al 1996) and Taiwan (Deahl et al 2002), rather than as a result of in situ selection of metalaxyl resistance. The vast majority (97%) of isolates from potato belonged to a single multilocus genotype, JE-1, or a variant thereof.…”