Pathotype IV, a New and Highly Virulent Pathotype of Didymella rabiei, Causing Ascochyta Blight in Chickpea in Syria

Abstract

The causal agent of Ascochyta blight disease of chickpea (Cicer arietinum L.) is highly variable because of the presence of a sexual phase (Didymella rabiei). There is also selection pressure on the pathogen due to wide adoption of improved resistant chickpea cultivars in some countries. The pathogen is able to produce pathotypes with specific virulence on particular cultivars. Three pathotypes, I, II, and III, have been reported (3). In this study, we confirmed the presence of a new and highly virulent pathotype that we designate as pathotype IV. To test the pathogenicity of the isolates collected and maintained at ICARDA, 10 isolates representing a wide spectrum of pathogenic variation, including those classified by S. M. Udupa et al. (3) and a putatively identified more virulent type, which was collected from a chickpea production field in the Kaljebrine area, Syria, were inoculated onto a set of differential chickpea genotypes. The differential genotypes, ILC 1929, ILC 482, ILC 3279, and ICC 12004, were sown in individual 10-cm-diameter pots containing potting mix and arranged in a randomized block design with three replications in a plastic house maintained at 18 to 20°C. Each differential genotype was inoculated individually with the 10 isolates following the methodology of S. M. Udupa et al. (3). DNA was extracted from single-spored isolates to compare the genotypes of the isolates using three simple sequence repeat (SSR) markers (ArA03T, ArH05T, and ArH06T) (2) and to determine the frequency of mating types (MAT) through the use of MAT-specific PCR primers for MAT1-1 and MAT1-2 (1). Host genotype reactions were measured on a 1 to 9 rating scale (1 = resistant and 9 = plant death). On the basis of the pathogenicity tests, the isolates were classified into four pathotypes: I (least virulent, killed ILC 1929 but not ILC 482, ILC 3279, or ICC12004); II (virulent, killed ILC 1929 and ILC 482 but not ILC 3279 or ICC12004); III (more virulent, killed ILC 1929, ILC 482, and ILC 3279 but not ICC12004); and IV (highly virulent, killed all four host differentials). Of 10 single-spore isolates tested, four showed similar disease reactions unique to pathotype I, four revealed pathotype II reactions, and one isolate each behaved like pathotype III or pathotype IV. SSR fingerprinting of these isolates provided evidence for genetic diversity since SSR ArH05T was highly polymorphic and amplified five bands, including pathotypes III- and IV-specific bands, which need further investigation to discern if this locus has any role to play in the virulence. MAT-type analysis showed that seven isolates were MAT1-1 while the remaining three isolates were MAT1-2. Only pathotype I showed the profile of MAT1-2 and the other three pathotypes were MAT1-1. Initially, a number of chickpea wild relatives were screened to identify sources of resistance to pathotype IV, but none of the accessions tested showed resistance. However, efforts are underway to combine minor and major gene(s) available in the breeding program in addition to a further search of the wild gene pools to control pathotype IV. References: (1) M. P. Barve et al. Fungal Genet. Biol. 39:151, 2003. (2) J. Geistlinger et al. Mol. Ecol. 9:1939, 2000. (3) S.M. Udupa et al. Theor. Appl. Genet. 97:299, 1998.

Genetic and Pathogenic Variability of Ascochyta rabiei Isolates from Pakistan and Syria as Detected by Universal Rice Primers

“…SSR marker ArH05T was recently reported to amplify Syrian pathotypes III and IV specific bands [4] while in our study two other SSR markers (ArA06T and ArH02T) also differentiated Syrian pathotypes III from IV but unable to distinguish PAR from SAR (Figure 2a). On the other hand the URP primers were highly polymorphic and not only differentiated least aggressive pathotype I (PAR 4) from rest of highly aggressive pathotypes III and IV but also differentiated PAR from SAR (Figure 2b).…”

“…Pathotype variability is necessary to select the appropriate pathotype for screening genotypes in resistance breeding programme [2]. Differentiation of Ascochyta rabiei (AR) into 3 classes (pathotype I, II and III) was reported in Syria and has been widely accepted [3] and recently highly aggressive pathotype IV has been reported by Imtiaz et al [4]. In Pakistan three pathotypes were also identified by Jamil et al [5] and Ali et al [6] using chickpea differential genotypes (ILC1929, ILC482 and ILC3279) and (Spanish white, Dwelley and ICC12004) respectively.…”

“…Previous studies were based on RAPD and SSR markers for the assessment of genetic diversity of AR isolates [3,5,6,[10][11][12][13]. Only SSR markers were reported by Imtiaz et al (2011) to differentiate pathotype III and IV from Syria.…”

Effect of integrated management on Fusarium wilt progression and grain yield of chickpea in Syria

“…Chickpea sowing during early spring could expose the crop to terminal heat and moisture stress. Although farmers in Syria have widely adopted early winter (December) sowing of chickpea, some of them have started sowing their chickpea in early (January) mainly due to weed problem and as a precautionary measure to avoid high Ascochyta blight disease pressure that affects chickpea due to the appearance of new virulent pathotypes of D. rabiei (Imtiaz et al 2011). Though variability in wilt incidence was observed across locations and seasons, our results clearly showed that early sowing can provide good yield.…”

An Update on Genetic Resistance of Chickpea to Ascochyta Blight

“…A new A. rabiei pathotype (pathotype IV) was reported in Syria that is capable of affecting the highly resistant chickpea genotypes (ICC-12004 and ICC-3996) known for their resistance to pathotypes I, II and III. Breeding materials at ICARDA are being screened against this new pathotype IV, and so far low levels of resistance have been observed [37,38]. High genetic diversity has also been reported from USA, Tunisia and Canada where popular varieties have become susceptible to new aggressive pathotypes [26][27][28].…”