Genetic analysis of karnal bunt resistance in 14 Mexican bread-wheat genotypes

Fourteen Mexican genotypes of bread wheat (Triticum aestivum L.) with good to moderate levels of resistance to Karnal bunt (Tilletia indica (Mitra)) were crossed with the highly susceptible cultivar WL711 to determine the genetic basis of resistance. The parents, F₁ F₂ and backcross populations of the 14 crosses were evaluated under artificial epiphytotic conditions during the 1993–94 season for Karnal bunt resistance. The F₁ data suggested that the resistance was dominant to partially dominant over susceptibility. The F₂ analysis of the segregation ratios in the F₂ and backcross generations indicated that the resistance in the wheat genotypes Luan, Attila, Vee #7/Bow, Star, Weaver, Milan, Sasia and Turacio/Chil is controlled by two genes. The resistance in genotypes Cettia, Irena, Turaco, Opata, Picus, and Yaco was found to be conditioned by a single dominant gene. The genotypes with two genes for resistance expressed a higher level of resistance than those with a single gene and, therefore, are better sources of resistance to Karnal bunt.     

Genetic analysis of resistance to Karnal bunt (Tilletia indica,Mitra) in bread wheat

Summary Karnal bunt caused by Tilletia indica in wheat seriously affects the quality of the grains. It is important to generate information on the genetics of resistance to this pathogen so as to aid resistance breeding. For this purpose, four Karnal bunt-resistant lines from China, Brazil and CIMMYT (International Maize and Wheat Improvement Center) and a susceptible Indian cultivar, WL711, were used. The parents, F1 and F3 progenies of five parental diallel crosses revealed that independently segregating loci with three partial dominant resistance alleles were involved in the resistance of Karnal bunt. Lines RC7201/2^*BR2 and Roek//Maya/NAC carried one locus for resistance while Shanghai#7 and Aldan/IAS58 have two and three loci, respectively. One common locus was present in all four resistant parents, which imparted a high level of resistance.     

Monosomic analysis of Helminthosporium leaf blight resistance genes in wheat

A set of 21 monosomic (2n ‐ 1) and the disomic (2n) lines of the ‘Chinese Spring’ cultivar were crossed with ‘Chirya‐3′, the CIMMYT synthetic wheat line which has been identified as highly resistant for Helminthosporium leaf blight disease (HLB), in order to locate the genes governing disease resistance. The F₁ and segregating populations were challenged and screened against the most virulent pure mono‐conidial HLB isolate KL‐8 (Karnal, India). The F₁ progenies of the crosses were found to be susceptible because of the recessive nature of resistance. The F₂ progeny of the control cross (‘Chinese Spring’בChirya‐3’), segregated in the ratio of 1: 15 (resistant: susceptible), indicating that resistance to HLB was controlled by a pair of recessive genes. While the F₂ progeny of 19 monosomic crosses segregated in the ratio of 1: 15 (resistant: susceptible), the progeny of the remaining two crosses, 7B and 7D, deviated significantly from the ratio, revealing that 7B and 7D were the critical chromosomes for resistance genes that were located one on each chromosome. Moreover, the critical lines, 7B and 7D, confirmed the digenic complementary recessive nature of gene action by fitting well with the overall pooled F₂ segregation ratio of 13: 51 (resistant: susceptible) as expected for digenic complementary recessive resistance. The F₃ segregation ratios of the critical crosses, based on their pooled F₂ analysis, was estimated as 19: 32: 13 (non‐segregating susceptible: segregating as susceptible and resistant: non‐segregating resistant). F₃ progenies when tested with these ratios showed goodness‐of‐fit, confirming that the two pairs of recessive resistance genes were located on chromosomes 7B and 7D.     

Inheritance of Karnal bunt-free trait in bread wheat

A Karnal bunt (KB)‐free wheat stock (‘KBRL22’) obtained from a cross of two resistant lines (‘HD29’ and ‘W485’) was used as a donor to introgress the KB‐free trait into ‘PBW343’(an ‘Attila’ sib), the most widely grown wheat cultivar in India. The number of KB‐free and KB‐affected plants in BC ₁, BC₂, BC₃ and BC₄ as well the F₂ was recorded after artificial inoculations. The segregation pattern in these generations clearly indicated two independently segregating, dominant genes which jointly confer the KB‐free attribute. The importance of the KB‐free line generated in this experiment is discussed.     

Inheritance of resistance to Tilletia indica (Mitra) in synthetic hexaploid wheat ×Triticum aestivum crosses

Inheritance of resistance to Karnal bunt was investigated in the crosses of four resistant synthetic hexaploid wheats (SH; Triticum turgidum×T. tauschii) and two susceptible T. aestivum cultivars. The resistance was dominant or partly dominant over susceptibility. The SH cultivars Chen/T. tauschii (205) and Chen/T. tauschii (224) have single dominant resistance genes which could be allelic to each other. ‘Altar 84’/T. tauschii (219) appeared to have two dominant genes for resistance. ‘Duergand’T. tauschii (214) possessed two complementary dominant genes for resistance. The work is being extended to involve diverse Karnal bunt-resistant SH and bread wheat cultivars.     

Potential use of doubled haploid lines for the screening of resistance to yellow rust (Puccinia striiformis) in hexaploid wheat

Doubled haploid lines derived from anther culture of two Iranian spring wheat genotypes‘Ghods’susceptible and‘9106’resistant to yellow rust in Iranian field conditions, and their F₁ hybrids were used in this study. Seedlings of 36 doubled haploid lines, selected out of 96 according to their agronomic traits and the two parental genotypes were inoculated with eight races of yellow rust. The parental genotypes (‘Ghods’and‘9106’) were segregating for some of the races but their doubled haploid lines were either resistant or susceptible to them.‘Ghods’was susceptible to three of the races studied but three doubled haploid lines derived from it were resistant to them. Five selected doubled haploids from the‘9106’genotype and six from F₁ hybrid plants were resistant to all eight races tested. After further investigations in Iranian field conditions it was found that some of these lines can be used as donor genotypes for resistance to yellow rust in wheat breeding programmes. Use of these genotypes should be possible if the French yellow rust races used for selection also represent the dominant races in Iran. It can be concluded that anther culture provides an efficient method for fixing genes of resistance to yellow rust and desirable doubled haploids from F₁ plants can be derived.     

Resistance to Karnal bunt in Hordeum chilense and its amphiploids with Triticum species

Reactions of Hordeum chilense accessions H1 and H7 and their amphiploids, HT8, HT9 and HT28 (named as tritordeum) alongwith wheat lines, T22, T24 and T59 used in their synthesis, were studied for resistance to the Karnal bunt pathogen (Tilletia indica) of wheat. Both the accessions of H. chilense and one tritordeum line, HT8, were rated as highly resistant with zero co-efficient of infection, whereas the other two tritordeum lines HT28 and HT9 were rated as moderately susceptible and susceptible with 5.2 and 10.5 co-efficients of infection, respectively, compared to reaction of the wheat lines involved in their synthesis. Karnal bunt infection was maximum on the susceptible wheat cultivar WL-711 with 24.3 co-efficient of infection. All the wheat lines involved in the synthesis of amphiploids were susceptible to Karnal bunt except, T59 (Triticum sphaerococcum) (6X), which showed a moderate level of resistance. This revised version was published online in July 2006 with corrections to the Cover Date.     

Synthetic Amphiploids of Wheet as a ource of Resistance to Karnal Bunt (Neovossia Indica)

Twelve synthesized ainphiplonds involving Karnal bunt (Neovossia indica)-resisiant accessions of Triticum monococum, T. boeoticum and Aegilops sqiwrrosa and susceptible but otherwise well adapted and high yielding T. Durum cultiviars were evaluated for Karnal bunt resisiance under artificial inoculation conditions. All ihe synthetic amphiploids, except DWI. 5031 x T. monocoirtum aniphlploid, were free from Karnal bunt disease indicating that the Karnal bunt resistance or T. motsococcum, T. boeoticMrn and Ae, squarrosa is expressec in the presence of the dnrum complement. The importance and utilization of the amphiploids fox breeding wheat varieties resistant to karnal bunt are discussed.     

Genetic Relationships Among Four Pepper Genotypes Resistant to Phytophthora capsici

According to our previous investigations, resistance to Phytophthora capsid in Capsicum annuum genotypes, ‘Line 29’, ‘PI201232’, ‘PI201234’ and Serrano Criollo de Morelos 334 (‘SCM334’), seems to be controlled by three genes. In order to determine the genie relationships between these four sources of resistance, three experiments were conducted which included the four genotypes, their F₁s, F₂s, F3s and BC₁ generations together with the susceptible pepper genotype ‘Morron INI A 224’. Inoculations were made, when plants had 4—6 leaves, by irrigating the culture substrate with a zoospore suspension of P. capsici isolate ‘Bl’. Though the four genotypes showed percentages of resistance close to a 100%, none of them actually reached this level in the three experiments. ‘SCM334’ was the most resistant genotype, transmitting a high level of resistance to its F₁, F₂ and BQ generations. ‘Line 29’ was more resistant than ‘PI201232’ and ‘PI201234’. However, the F₁ F₂ and BQ generations of these three lines showed similar degrees of resistance. The four genotypes seem to have one of the three genes postulated for their resistance in common. All genes displayed a similar level of resistance, except the specific genes of ‘SCM334’, the effect of which was slightly higher. Several working procedures are suggested for breeding programmes.     

Inheritance of resistance to Fusarium wilt (race 2) in chickpea

The inheritance of resistance to Fusarium wilt (race 2) of chickpea was studied in a set of three crosses, i.e. ‘WR315’בC104’ (resistant × susceptible), ‘WR315’בK850’ (resistant × tolerant) and ‘K850’בGW5/7’ (tolerant × tolerant) in order to investigate the number of genes involved, their complementation and to find out whether resistant segregants are possible in a cross between two tolerant cultivars. Tests of F₁, F₂ and F₃ generations of these crosses under controlled conditions at ICRISAT, Patancheru, India, indicated involvement of three loci (two recessive and one dominant alleles). The homozygous recessive form at the first two loci conferred resistance whereas susceptibility occurred when the first two loci were in the dominant form. A dominant allele at the third locus can complement the dominant alleles at the other two loci to confer tolerance. Occurrence of resistant segregants in a cross between two tolerant cultivars was observed.     

Inheritance of resistance to spot blotch caused by Bipolaris sorokiniana in spring wheat

Three F₁ progenies and their families in the segregating generations (F₃, F₄, F₅ and F₆), obtained after crossing resistant × susceptible wheat genotypes were studied in the field to determine the genetics of resistance to spot blotch caused by Bipolaris sorokiniana. Spot blotch scores in the F₁ generation showed absence of dominance. Individually threshed F₂ plants were used to advance the generations. Progenies (200‐250) of resistant genotypes Acc. No. 8226, Mon/Ald, Suzhoe#8 crossed with susceptible ‘Sonalika’ were evaluated in the F₃, F₄, F₅ and F₆ generations under induced epiphytotic conditions. Based on disease score distribution in individual progeny rows, F₃ progenies were grouped into four classes: homozygous resistant, homozygous susceptible, segregating resistant and segregating susceptible. Resistance appeared to be under the control of three additive genes. The presence of three genes was also noted in the distribution of F₄ and F₅ lines. In the case of F₆ progeny rows, both quantitative and qualitative models were used to estimate the number of segregating genes based on a 2‐year trial. It appeared that resistance to spot blotch was controlled by the additive interaction of more than two genes, possibly only three.     

Genetics of resistance to Karnal bunt disease of wheat

Inheritance of resistance to Neovossia indica was studied in a Triticum aestivum line HD 29. To overcome the influence of environment on disease expression, the study was conducted by extensive evaluation of advanced generation (F8) recombinant inbred lines (RILs) developed by single seed descent from the cross WL 711 (susceptible) × HD 29 (resistant. The results suggested that HD 29 possesses three major genes for resistance to isolated Ni7 and two genes for resistance to isolate Ni8. One of the two genes controlling resistance to Ni8 is common with one of the genes conferring resistance to Ni7. These observations have important implications in breeding for Karnal bunt resistance.     

Recessive genes controlling resistance to Helminthosporium leaf blight in synthetic hexaploid wheat

A study was conducted under controlled environment conditions in a phytotron to determine the nature of the inheritance of resistance Helminthosporium leaf blight (HLB) in a synthetic hexaploid wheat line, ‘Chirya‐3’, against the isolate KL‐8 of Bipolaris sorokiniana from the major wheat growing region of India. Crosses were made between two susceptible lines ‘WH 147’ and ‘Chinese Spring’. Analyses of F₁ and F₂ populations of these two crosses (‘WH 147’בChirya‐3’ and ‘Chinese Spring’בChirya‐3’) showed that resistance against the isolate in ‘Chirya‐3’ was governed by two recessive genes functioning in a complementary interaction giving an F₂ segregation pattern of 1 : 15 (resistant : susceptible). The segregation pattern of the resistant F₂ progenies in F₃ families from both crosses confirmed that two homozygous recessive genes were responsible for resistance to the isolate of Bipolaris sorokiniana in the synthetic line ‘Chirya‐3’. It is proposed that the genes be designated as hlbr1 and hlbr2.     

Histological and inheritance studies of partial resistance in the Brassica napus–Albugo candida host-pathogen interaction

Traditional and doubled haploid (DH) genotypes of oilseed Brassica spp. resistant, partially resistant, moderately susceptible, and susceptible to Albugo candida were compared for phenotypic development of host‐pathogen interaction and histology of host‐pathogen interaction. The partially resistant genotype showed pinhead‐size pustules, mainly on the upper surface of cotyledonary leaves. Relatively less mycelium was observed in the partially resistant genotype compared with the susceptible genotype. In resistant B. napus genotypes, there was neither pustule development nor any mycelial growth. In the moderately susceptible genotype, the pustules were similar to those in the partially resistant genotype in being of pinhead‐size and occasionally coalescing. However, ample mycelial growth in the mesophyll tissue in the moderately susceptible genotype was similar to that in the susceptible control B. rapa cv. ‘Torch’. The susceptible genotype B. rapa cv. ‘Torch’ also showed large coalescing pustules. In the non‐host B. juncea cv. ‘Commercial Brown’, no pustules were formed although some mycelial growth was observed beneath the epidermal cell layer and in the mesophyll cell layer of the cotyledonary leaf tissue. For inheritance studies, two partially resistant B. napus genotypes were crossed with a resistant B. napus genotype. Various generations viz., F1, F1(reciprocal), F₂, and DHs produced from the crosses were inoculated with a zoospore suspension of race 7v of A. candida. The partially resistant phenotype appeared to be controlled by a single recessive gene designated as wpr with variable expression. The simple inheritance of partial resistance has implications for disease resistance breeding against white rust, as this type of resistance can be easily incorporated into elite breeding lines through conventional and DH breeding methods.     

Inheritance of insensitivity to culture filtrate of Pyrenophora tritici-repentis, race 2, in wheat (Triticum aestivum L.)

Tan spot of wheat is caused by the fungus Pyrenophora tritici‐repentis. On susceptible hosts, P. tritici‐repentis induces two phenotypically distinct symptoms, tan necrosis and chlorosis. This fungus produces several toxins that induce tan necrosis and chlorosis symptoms in susceptible cultivars. The objectives of this study were to determine the inheritance of insensitivity to necrosis‐inducing culture filtrate of P. tritici‐repentis, race 2, and to establish the relationship between the host reaction to culture filtrate and spore inoculation with respect to the necrosis component. The F₁, F₂, and BC₁F₁ plants and F_2:8 lines of five crosses involving resistant wheat genotypes ‘Erik’, ‘Red Chief’, and line 86ISMN 2137 with susceptible cultivars ‘Glenlea’ and ‘Kenyon’ were studied. Plants were spore‐inoculated at the two‐leaf stage. Four days later, the newly emerged uninoculated third leaf was infiltrated with a culture filtrate of isolate Ptr 92–164 (race 2). Reactions to the spore inoculation and the culture filtrate were recorded 8 days after spore inoculation. The segregation observed in the F₂ and BC₁F₁ generations and the F_2:8 lines of all crosses indicated that a single recessive gene controlled insensitivity to necrosis caused by culture filtrate. This gene also controlled resistance to necrosis induced by spore inoculation.     

Genetic analysis of gene‐specific resistance to mungbean yellow mosaic virus in mungbean (Vigna radiata)

Six intervarietal crosses involving two resistant and three susceptible genotypes of mungbean were attempted with the objectives to determine the mode of inheritance of gene‐specific Mungbean Yellow Mosaic Virus (MYMV) resistance. An infector row technique along with artificial inoculation was used for evaluating parents, F₁, F₂ and F₃ plants for MYMV resistance. Disease scoring for MYMV indicated that F₁s were highly susceptible as were the susceptible parents while resistant parent exhibited resistant reaction. The F₂ progeny segregated in the ratio of 9 S:3 MS:3 MR:1 R suggesting that the resistance was governed by digenic recessive genes (r_m1 and r_m2). When one gene (r_m1) was present in the homozygous recessive condition in different plants, it conferred moderately susceptible (MS) reaction, whereas when other gene (r_m2) was in homozygous condition, moderately resistant (MR) reaction was obvious. When both genes (r_m1 and r_m2) were present together in the homozygous recessive condition, resistant reaction (R) was observed. The F₂ segregation explained on the basis of phenotypic expression was further confirmed by F₃ segregation.     

Molecular mapping of two recessive genes controlling resistance to bacterial leaf pustule disease in soybean (Glycine max)

Bacterial leaf pustule (BLP) caused by Xanthomonas axonopodis pv. glycines (Xag) is a serious soybean disease. A BLP resistant genotype ‘TS-3’ was crossed with a BLP susceptible genotype ‘PK472’, and a segregating F₂ mapping population was developed for genetic analysis and mapping. The F₂ population segregation pattern in 15:1 susceptible/resistance ratio against Xag inoculum indicated that the resistance to BLP in ‘TS-3’ was governed by two recessive genes. A total of 12 SSR markers, five SSR markers located on chromosome 2 and seven SSR markers located on chromosome 6 were identified as linked to BLP resistance. One of the resistance loci (r1) was mapped with flanking SSR markers Sat_183 and BARCSOYSSR_02_1613 at a distance of 0.9 and 2.1 cM, respectively. Similarly, SSR markers BARCSOYSSR_06_0024 and BARCSOYSSR_06_0013 flanked the second locus (r2) at distances of 1.5 and 2.1 cM, respectively. The identified two recessive genes imparting resistance to BLP disease and the SSR markers tightly linked to these loci would serve as important genetic and molecular resources to develop BLP resistant genotypes in soybean.     

Characterization of broad‐spectrum resistance to Soybean mosaic virus in soybean [Glycine max (L.) Merr.] cultivar ‘RN‐9’

Soybean mosaic virus (SMV) can cause serious yield losses in soybean. Soybean cultivar ‘RN‐9’ is resistant to 15 of 21 SMV strains. To well‐characterize this invaluable broad‐spectrum SMV‐resistance, populations (F₁, F₂ and F_2:3) derived from resistant (R) × susceptible (S) and R × R crosses were tested for SMV‐SC18 resistance. Genetic analysis revealed that SC18 resistance in ‘RN‐9’ plus two elite SMV‐resistant genotypes (‘Qihuang No.1’ and ‘Kefeng No.1’) are controlled by independently single dominant genes. Linkage analysis showed that the resistance of ‘RN‐9’ to SMV strains SC10, SC14, SC15 and SC18 is controlled by more than one gene(s). Moreover, Rsc10‐r and Rsc18‐r were both positioned between the two simple sequence repeats markers Satt286 and Satt277, while Rsc14‐r was fine‐mapped in 136.8‐kb genomic region containing sixteen genes, flanked by BARCSOYSSR_06_0786 and BARCSOYSSR_06_0790 at genetic distances of 3.79 and 4.14 cM, respectively. Allelic sequence comparison showed that Cytochrome P450‐encoding genes (Glyma.06g176000 and Glyma.06g176100) likely confer the resistance to SC14 in ‘RN‐9’. Our results would facilitate the breeding of broad‐spectrum and durable SMV resistance in soybeans.     

Inheritance and allelism of wheat streak mosaic virus resistance in two Iranian wheat lines

Wheat streak mosaic (WSM) caused by wheat streak mosaic virus (WSMV) is a serious disease of wheat and many plants in the grass family. In previous studies genotypes collected from different parts of Iran, were screened for WSM resistance. Two resistant genotypes, “Adl Cross” and “4004” were crossed to one susceptible genotype “Marvdasht.” Reciprocal crosses were also made. Seedlings of parents, F₁, F₂, backcrosses to susceptible (BCS) and resistant (BCR) were evaluated for WSMV reaction based on scales 0–7, by artificial infection under greenhouse conditions. Allelism was studied by evaluating the F₁ and F₂ seedlings of the resistant × resistant cross. Inheritance of resistance to WSMV in Adl Cross and 4004 was controlled by one dominant gene. No allelism was observed between resistance genes. Among the F₂ seedlings of the resistant × resistant cross relatively more resistant genotypes with a zero score were observed. These two genes, therefore, can be incorporated into an adapted wheat cultivar to produce a more durable resistance.     

Development of RAPD markers associated with common bunt resistance to race T1 (Tilletia tritici) in spelt wheat

Common bunt caused by Tilletia tritici and T. laevis has occurred worldwide and reduces yield and quality in common and durum wheats. The development of DNA markers linked to bunt resistance to race T1 in the cross, ‘Laura’(S) בRL5407’ (R), was carried out in this study based on the single head derived F_4:5 and single seed derived F_4:6 populations. Bulked segregant analysis was used to identify two random amplified polymorphic DNA (RAPD) markers linked to the gene for resistance to race T1 in the spelt wheat ‘RL5407′. The two markers identified, UBC548₅₉₀ and UBC274₉₈₈, flanked the resistance gene with a map distance of 9.1 and 18.2 cM, respectively. The former was linked in repulsion phase to bunt resistance while the later was in coupling phase. The two RAPD markers and the common bunt‐resistance gene all segregated in Mendelian fashion. Use of these two RAPD markers together could assist in incorporating the bunt‐resistance gene from spelt wheat into common wheat cultivars by means of marker‐assisted selection.