Genetic analysis of durable powdery mildew resistance in a common wheat line
2002; BioMed Central; Volume: 136; Issue: 3 Linguagem: Inglês
10.1034/j.1601-5223.2002.1360304.x
ISSN1601-5223
AutoresHilma Peusha, T. V. Lebedeva, O. Priilinn, T. Ėnno,
Tópico(s)Plant pathogens and resistance mechanisms
ResumoHereditasVolume 136, Issue 3 p. 201-206 Open Access Genetic analysis of durable powdery mildew resistance in a common wheat line HILMA PEUSHA, HILMA PEUSHA Estonian Agricultural University, Institute of Experimental Biology, Department of Plant Genetics, Harku, EstoniaSearch for more papers by this authorTATJANA LEBEDEVA, TATJANA LEBEDEVA The N.I. Vavilov Institute of Plant Industry, Sankt-PetersburgSearch for more papers by this authorOSKAR PRIILINN, OSKAR PRIILINN Estonian Agricultural University, Institute of Experimental Biology, Department of Plant Genetics, Harku, EstoniaSearch for more papers by this authorTAMARA ENNO, TAMARA ENNO Estonian Agricultural University, Institute of Experimental Biology, Department of Plant Genetics, Harku, EstoniaSearch for more papers by this author HILMA PEUSHA, HILMA PEUSHA Estonian Agricultural University, Institute of Experimental Biology, Department of Plant Genetics, Harku, EstoniaSearch for more papers by this authorTATJANA LEBEDEVA, TATJANA LEBEDEVA The N.I. Vavilov Institute of Plant Industry, Sankt-PetersburgSearch for more papers by this authorOSKAR PRIILINN, OSKAR PRIILINN Estonian Agricultural University, Institute of Experimental Biology, Department of Plant Genetics, Harku, EstoniaSearch for more papers by this authorTAMARA ENNO, TAMARA ENNO Estonian Agricultural University, Institute of Experimental Biology, Department of Plant Genetics, Harku, EstoniaSearch for more papers by this author First published: 04 November 2002 https://doi.org/10.1034/j.1601-5223.2002.1360304.x Hilma Peusha, Estonian Agricultural University, Institute of Experimental Biology, Department of Plant Genetics, 76902 Harku, Estonia. E-mail: ebi @ ebi.ee AboutSectionsPDF ToolsExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Abstract Genetic studies using monosomic and hybridological analyses had confirmed that resistance of a common wheat line k-15560 to powdery mildew in seedling stage was conditioned by one dominant gene located on chromosome 7B, and resistance in adult stage was controlled by two dominant genes. Cytological analysis of meiosis in the F1 monosomic hybrids has revealed reciprocal translocation involving chromosomes 2A/7A. In the F1 monosomic hybrids genes, causing a decrease in pairing were found on chromosomes 3B and 4D, and genes enhancing pairing – on chromosomes 2A and 3A. Powdery mildew caused by the obligate fungus Erysiphegraminis (Blumeriagraminis) DC f. sp. tritici Em Marchal is one of the most important diseases of wheat (Triticumaestivum L. em Thell) in temperate climates. The most economical and enviromental way for powdery mildew control remains development of resistant cultivars. Up to now 28 gene loci (Pm) for resistance against powdery mildew have been assigned to particular wheat chromosomes (McIntosh et al. 1998; Järve et al. 2000; Peusha et al. 2000). In order to improve powdery mildew resistance, attempts have been made to pyramide several Pm genes in one cultivar, nevertheless, no durable resistance has been provided (Brown et al. 1997). Due to the occurrence of new pathogenic virulence or ineffective adult resistance, only some resistance genes are useable for wheat breeding in Europe. Many wheat cultivars seem to have the same few Pm genes-Pm2, Pm4b, Pm5, Pm6, Pm8 (Zeller et al. 1993a; McIntosh et al. 1998), providing little protection against the contemporary pathogen populations (Limpert et al. 1987). It has been shown that, as a rule, resistance during plant ontogeny was controlled by different genes. In wheat cv. Axminster resistance to powdery mildew in seedling stage is conferred by one gene, and in adult stage by two genes (Ray et al. 1954). Different responses of wheat plants on pathogen infection during ontogeny were observed in cultivars Asosan (Pm 3a) and Chul (Pm 3b) (Favret et al. 1983). In this study an attempt has been made to determine inheritance mode and chromosomal location of the genes conferring durable resistance to powdery mildew in common wheat line k-15560. The cytological analysis of the chromosome pairing at meiosis in monosomic hybrids F1 Chinese Spring×k-15560 has been carried out to reveal chromosomes involved in reciprocal translocations. MATERIALS AND METHODS Plant material and resistance analysis Resistant to powdery mildew common wheat line was selected from landrace after laboratory and field assessments at the Derbent Experimental Breeding Station, Dagestan, Transcaucasia (Lebedeva 1991, 1994) and its high immunity has been retained during more than two decades. The sample of this line was included into the World Wheat Collection of the Vavilov Institute of Plant Industry, St. Petersburg, as specimen k-15560. For determination of the resistance inheritance mode and number of genes conferring resistance, line k-15560 was crossed with the susceptible wheat cultivars Diamant and Chinese Spring and with the resistant cultivars Weihenstephan M1, Halle stamm 13471 and line CI 12632. The hybrid progenies F1 and F2 were estimated for mildew resistance at ear emergence time in field conditions under natural infection with the native population of pathogen. Assessment of the F3 progeny was performed in seedling stage after inoculation with the same natural population of pathogen. The method of inoculation, conditions of inoculation and disease assessment were according to Zeller et al. (1993b). Reaction was scored 10 days after inoculation when the susceptible cultivars were heavily infected, using a 0, 0; and 1–4 scale, where 0 represents no visible symptoms, 0; necrotic spots, and 3–4 highly susceptible reactions (Mains and Dietz 1930). Monosomic analysis and powdery mildew test The set of 21 monosomic lines of cv. Chinese Spring, used for resistance gene location, was obtained from Prof. F. Zeller, Technische Universität München, Institut für Pflanzenbau und Pflanzenzüchtung, Freising – Weihenstephan, Germany. Monosomic plants were identified by somatic chromosome counts on excised root tips, pretreated in ice water and prepared by the Feulgen procedure. Cytologically identified monosomic plants of Chinese Spring lines were crossed with plants of line k-15560. Cytologically verified monosomic F1 plants from each cross were self-pollinated and segregation ratios of their F2 progenies for mildew resistance were analyzed using the χ2 test. The Erysiphe graminis isolates no. 10 (virulent to Pm3d, Pm4a and Pm8 and avirulent to Pm1, Pm2, Pm3a, Pm3b, Pm3c, Pm4b, Pm5, Pm6 and Pm1+Pm2+Pm9) and no. 12 (virulent to Pm1, Pm2, Pm3a, Pm3c, Pm5, Pm6, Pm1+Pm2+Pm9 and avirulent to Pm3b, Pm3d, Pm4a, Pm4b, Pm8) were used to postulate and differentiate the resistance genes in line k-15560. These isolates were selected from single-spore progenies collected in Europe and kindly provided by Dr. F. Felsenstein, Institut für Pflanzenbau und Pflanzenzüchtung, Freising–Weihenstephan, Germany. The test for mildew resistance was carried out on segments of 10-day-old primary leaves of host seedlings grown in a phytotron. The leaf segments were cultured in Petri-dishes on 6 g/l agar and 35 mg/l benzimidazole according to the methods described by Lutz et al. (1992). Inoculum was first produced on leaf segments of cv. Kanzler and spread in a setting tower onto the plant material at densities of 400–500 spores/cm2. Disease reaction was assessed 10 days after inoculation. Three main classes of host reactions were distinguished: r=resistant (0–20 % infection relative to susceptible cv. Kanzler); i=intermediate (30–50% infection); s=susceptible (>50 % infection). Method for inoculation of leaf segments and disease assessment were used according to Hsam and Zeller (1997). Cytological analysis The somatic chromosome numbers of the parental and F1 plants were determined in root-tip cells using standard Feugen staining procedures. Spikes from F1 plants were collected to determine the mode of chromosome behaviour during the first meiotic division (MI). They were fixed in alcohol-glacial acetic acid: (3:1) solution for 48 h and stored under refrigeration (4°C) in 70 % alcohol until used. Anthers were stained in alcohol-acid-carmine for 48 h and squashed in 45 % acetic acid. Meiotic chromosome pairing in pollen mother cells (PMC) was analyzed at metaphase I using microscope "Axioskop" (Karl Zeiss). Every PMC was scored for the presence of univalents, bivalents and multivalents, and where multivalent associations occurred, the number of chromosomes involved and their configurations were recorded. Appearance of trivalent associations and absence of univalents at MI was used for identification of the chromosomal interchanges. RESULTS AND DISCUSSION Genetic analysis for resistance In the field trials cultivars Diamant and Chinese Spring showed susceptible reaction to native population of Erysiphe graminis f. sp. tritici with the infection types 3–4. All the F1 plants of the cross k-15560×Diamant in the phase of ear emergence were resistant to pathogen, which indicate a dominant inheritance of resistance. Analysis of the F2 populations showed segregation into 228 resistant and 18 susceptible plants, satisfactorily fitting the genetic ratio of 15:1 (15 resistant: 1 susceptible, χ2=0.48) and thereby conforming to a dominant digenic inheritance of resistance in adult stage. In the F3 progeny of this cross from 202 families 143 were resistant and 59 susceptible to pathogen in seedling stage (3:1, χ2=1.93). Results of this experiment evidenced that resistance of line k-15560 in seedling stage to native population of Erysiphe graminis was controlled by one dominant gene, and in adult stage by two dominant genes, one of which has retained its activity during plant ontogeny. The special studies were performed to analyse the genetic control of mildew resistance in wheat cultivars and lines by using near-isogenic lines of cv. Chancellor with known resistance genes (Briggle 1969). Results of these experiments showed that, besides the line k-15560, mildew resistance was manifested also in the cultivars/lines Weihenstephan M1 (Pm4b), Halle stamm 13471 (Pm3a), and CI 12632 (Pm2, Pm6). These cultivars/lines were crossed with each other and with susceptible cv. Diamant. Segregation ratios for the six cross-combinations in the F2 progeny showed clear differences in the resistance genes interactions (Table 1). Presented data showed that seedling-effective resistance of k-15560 was controlled by a single dominant gene, and resistance in adult stage conferred by two genes. Moreover, expression of one of these genes being prolonged during the whole plant ontogeny, and this gene is not identical to the genes Pm4, Pm6 and Pm3a (Lebedeva 1991, 1994). Table 1. Segregation for seedling reaction to mildew in F2 populations from various combinations of crosses between resistant and susceptible cultivars of common wheat Hybrid combination Number of plants Observed segregation χ2 χ2 Resistant Suscept. 3:1 15:1 k-15560×Diamant 553 426 127 1.21 Halle st.13471×Diamant 118 89 29 0.01 Weihenstephan M1×Diamant 188 146 42 0.70 k-15560×Weihenstephan M1 166 155 11 0.83 k-15560×Halle st.13471 157 146 11 0.15 Halle st.13471×Weihenstephan M1 270 252 18 0.06 Line (landrace) k-15560 has retained powdery mildew resistance during more than 20 years with infection of constantly changing population of pathogen. So far k-15560 has not been used in wheat practical breeding. Monosomic analysis In the crosses Chinese Spring×k-15560 the disomic F2 population tested against Erysiphe graminis isolates no. 10 and 12 segregated into 246:78 and 247:77, respectively, satisfactorily fitting a genetic ratio of 3 resistant:1 susceptible and thereby conforming to a dominant monogenic inheritance (Table 2). The segregation ratios of all F2 monosomic combinations, with the exception of that involving chromosome 7B, showed a ratio of 3:1 resistant to susceptible plants, corresponding to a dominant monogenic inheritance. Only the F2 population from the cross CSmono 7B×k-15560 deviated significantly (P<0.01) from the expected ratio of 3 resistant: 1 susceptible, indicating that one dominant gene is located on chromosome 7B (Table 2). 157 plants of the F2 progeny tested against isolate no. 10 segregated into 144 resistant: 13 susceptible plants (χ2=23.4), and the same F2 population tested against isolate no. 12 segregated into 141 resistant: 16 susceptible progenies (χ2=18.36). Such great deviation from Mendelian ratio of segregation with significant decrease of the amount of susceptible plants clearly indicated the location of the dominant gene for mildew resistance on the chromosome 7B. Table 2. Segregation for seedling reaction to mildew isolates no. 10 and 12 in monosomic F2 populations from crosses of Chinese Spring monosomics with common wheat line k-15560 Monosomic line Isolate no. 10 Isolate no. 12 Observed segregation χ2 Observed segregation χ2 Resist. Suscept. 3:1 Resist. Suscept. 3:1 1A 135 38 0.85 134 39 0.56 2A 121 42 0.05 126 37 0.46 3A 125 44 0.10 131 38 0.60 4A 113 37 0.01 121 29 2.57 5A 113 32 0.68 115 30 1.55 6A 117 30 1.65 118 29 2.18 7A 110 33 0.28 111 32 0.52 1B 112 33 0.39 115 30 1.44 2B 128 39 0.24 129 38 0.45 3B 102 34 0.00 106 30 0.63 4B 123 37 0.30 125 35 0.83 5B 102 33 0.58 105 30 0.55 6B 116 43 0.35 121 38 0.10 7B 144 13 23.40** 141 16 18.36** 1D 111 40 0.18 115 36 0.11 2D 75 21 0.50 75 21 0.50 3D 122 40 0.01 123 39 0.07 4D 119 33 0.87 115 37 0.03 5D 118 38 0.02 117 39 0.00 6D 63 18 0.33 62 19 0.10 7D 129 38 0.45 128 39 0.24 CSdis.x k-15560 246 78 0.15 247 77 0.25 **P<0.01. Only one powdery mildew resistance gene has been located to 7B chromosome – recessive gene Pm5 (McIntosh et al. 1998). This gene was first described by Mains (1934), subsequently located on chromosomal arm 7BL (Law and Wolfe 1966) and designated as Pm5 (Lebsock and Briggle 1974). The resistance gene Pm5 is prevalent in commercial cultivars and landraces grown in the Mediterranean region (McIntosh et al. 1967; Zeller et al. 1998). It is known that Pm5 occurs in tetraploid emmer wheat from which it was, probably, introduced into common wheat (Law and Wolfe 1966). But it is not known whether Pm5 is being transferred from tetraploid to hexaploid level in nature. The origin of resistance gene Pm5 could not be deduced, neither from wheat cultivars pedigrees, nor from additional data of same progenitors (Zeller et al. 1993a,b). It is most likely that Triticum dicoccum has been involved in the spontaneous hybridization with Triticum aestivum through natural outcrossing or unconscious selection. But the origin of gene conferring resistance in line k-15560 remains unknown. Multiple resistance genes may exist as an allelic series at a structurally simple locus. In wheat ten different alleles have been located at the Pm3 locus on chromosome 1AS (Zeller et al. 1993c; Zeller and Hsam 1998) and four alleles at the Pm1 locus on chromosome 7AL (Hsam et al. 1998). The Pm5 locus is composed of four different alleles –Pm5a in cv. Hope and Selpek, Pm5b in cv. Ibis and Kormoran, Pm5c in T. sphaerococcum line Kolandi and Pm5d in backcrossed-derived lines IGV1-455 and IGV2-556 (Hsam et al. 2001). According to authors, resistance gene Pm5a of cv. Hope in combination with other genes, such as Pm1c or Pm17 is very effective against the currently existing powdery mildew pathogenic races in Germany. Up to now, virulent mildew pathotypes to resistance gene Pm5d have not yet been detected in Europe. We can suppose that mildew resistance in line k-15560 may be conferred by one of the locus Pm5 dominant allele, or by an absolutely new effective gene. Meiosis The common wheat cultivars usually differ in their genomic and chromosomal structures, and these differences can express in various meiotic abnormalities, such as irregular chromosome pairing, multivalent formation, occurrence of reciprocal translocations etc (Baier et al. 1974; Vega and Lacadena 1982; Enno et al. 1998). Monosomic and disomic hybrids F1 Chinese Spring-mono×k-15560 were analyzed cytologically for meiotic behaviour at MI. Cytogenetical analysis of meiotic associations observed in the pollen mother cells at MI is shown in Table 3. In all monosomic hybrids F1 connections between chromosomes were rather weak with premature disjoining of the bivalents and increased number of additional univalents comparatively with the both parents. In the monosomic hybrids 3B and 4D the mean numbers of bivalents and chiasmata were lower, and that of univalents and rod bivalents were higher than in the other monosomic hybrids. The mean numbers of bivalents and chiasmata were greater and that of univalents and rod bivalents were lower in monosomic hybrids 2A and 3A. Among 21 monosomic hybrids tested monosomic lines 2A and 7A carried chromosomal translocation. As it is shown from the Table 3, hybrids F1 with monosomic lines 2A and 7A had trivalent configurations without univalents (0.97 and 1.30 %, respectively) and, consequently, these chromosomes involved in reciprocal translocation 2A/7A. Table 3. Chromosome pairing at MI of meiosis in monosomic hybrids F1 from crosses between Chinese Spring monosomics and line k-15560 Monosomic line No. of PMC Mean number per cell % of PMC with trivalents without univalents Number of PMCs with multi-valents Bivalents Univalents Chiasmata Multivalents 1III IIV Ring Rod Total 1A 82 16.5 3.0 19.50 1.90 36.07 0.024 – 2 (17–20)* (1–5) (33–39) (0–1) 2A 103 17.88 1.93 19.81 1.30 37.74 0.019 0.97 – 1 (18–20) (1–3) (35–40) (0–1) 3A 107 17.67 2.08 19.75 1.45 37.45 0.009 – 1 (17–20) (1–7) (30–40) (0–1) 4A 111 16.54 3.15 19.69 1.64 36.25 0.009 1 – (17–20) (1–7) (31–40) (0–1) 5A 62 17.00 2.62 19.62 1.63 36.71 0.032 1 1 (18–20) (1–5) (35–40) (0–1) 6A 69 17.29 2.16 19.45 2.05 36.73 0.014 1 – (17–20) (1–7) (29–40) (0–1) 7A 153 17.12 2.53 19.65 1.57 36.85 0.032 1.30 2 3 (17–20) (1–5) (32–40) (0–1) 1B 126 17.03 2.62 19.65 1.65 36.71 0.008 – 1 (18–20) (1–5) (33–40) (0–1) 2B 55 16.70 2.53 19.23 2.03 36.30 0.127 1 6 (17–20) (1–7) (34–40) (0–1) 3B 156 15.59 3.78 19.37 2.18 35.01 0.019 1 2 (17–20) (1–7) (30–40) (0–1) 4B 73 17.39 2.26 19.65 1.41 37.26 0.068 – 5 (16–20) (1–5) (32–40) (0–1) 5B 142 17.50 2.30 19.80 1.32 37.35 0.014 – 2 (18–20) (1–5) (33–40) (0–1) 6B 137 16.86 2.83 19.69 1.58 36.57 0.007 – 1 (17–20) (1–3) (32–40) (0–1) 7B 101 16.12 3.52 19.64 1.61 35.87 0.029 – 3 (18–20) (1–5) (35–40) (0–1) 1D 64 17.25 2.28 19.53 1.83 36.86 0.031 1 1 (18–20) (1–5) (34–40) (0–1) 2D 55 16.45 3.25 19.70 1.51 36.21 0.018 – 1 (18–20) (1–5) (36–40) (0–1) 3D 100 17.22 2.36 19.58 1.68 36.92 0.04 – 4 (16–20) (1–7) (30–40) (0–1) 4D 70 16.17 3.38 19.55 1.71 35.85 0.04 – 3 (18–20) (1–5) (35–40) (0–1) 5D 59 17.17 2.57 19.74 1.46 36.94 0.017 1 – (18–20) (1–5) (34–40) (0–1) 6D 96 16.73 2.83 19.56 1.78 36.35 0.03 3 – (18–20) (1–5) (36–40) (0–1) 7D 133 17.27 2.39 19.66 1.60 36.98 0.02 2 1 (18–20) (1–5) (34–40) (0–1) CSdis.x k-15560 148 17.68 2.91 20.59 0.50 38.31 0.013 1 1 (18–21) (1–4) (34–42) (0–1) * Range given in parentheses. 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