Hereditas 137: 186–197 (2002)

Resistance to scald (Rhynchosporium secalis) in barley (Hordeum�ulgare L.). II. Diallel analysis of near-isogenic linesVISHWANATH PATIL1, A� SMUND BJØRNSTAD1, HA� KON MAGNUS2 and JAMES MAC KEY3

1 Department of Horticulture and Crop Sciences, Agriculture Uni�ersity of Norway, A� s, Norway2 The Norwegian Crop Research Institute, A� s, Norway3 Department of Plant Biology, Swedish Uni�ersity of Agricultural Sciences, Uppsala, Sweden

Patil, V., Bjørnstad, A� ., Magnus, H. and Mac Key, J. 2002. Resistance to scald (Rhynchosporium secalis) in barley(Hordeum �ulgare L.). II. Diallel analysis of near-isogenic lines.—Hereditas 137: 186–197. Lund, Sweden. ISSN0018-0661. Received October 11, 2001. Accepted November 26, 2002

Near-isogenic lines (NILs) in the BC7 generation for resistance to barley scald (Rhynchosporium secalis Oudem. J.J. Davis)have been developed with ‘Ingrid’ as the recurrent parent (RP). Starting from 23 differential varieties and a classical BCprogram with disease tests followed by selection for the RP phenotype, NILs from the following 9 sources have beenselected for analysis: ‘Turk’, ‘Brier’, ‘CI 8162’, ‘La Mesita’, ‘Hispont’, ‘Atlas46’, ‘Modoc’, ‘Hudson’ and ‘Abyssinian’. The9 NILs were crossed in a half-diallel design. The NILs, their F1s and F2s were tested along with the donors and RPagainst R. secalis isolates ‘4004’ and ‘2’ to understand the degree of resistance in each NIL, allelism/linkage anddominance relationships among the NILs. With isolate ‘4004’, 13 of the 36 crosses segregated in the F2 generation. Acommon feature was that either ‘Atlas 46’-NIL or ‘Hudson’-NIL was one of the parents. Thus it seems that 7 out of the9 lines are allelic, probably at the Rrs1 complex locus on chromosome 3H, one carries the Rrs2 locus on chromosome 7Hand one is independent of both. Segregation with isolate ‘2’ was harder to establish because of a weak resistance gene inthe RP which acted additively with the other resistance genes and resulted in a narrower phenotypic range. Degree ofdominance/recessiveness depended on the crosses as well as the isolate used. In general GCA effects were much strongerthan SCA.

Åsmund Bjo�rnstad, Department of Horticulture and Crop Sciences, P.O. Box 5022, Agriculture Uni�ersity of Norway,NO-1432 A� s, Norway. E-mail: asmund.bjornstad@ipf.nlh.no

The imperfect fungus Rhynchosporium secalis [(Oud.)Davis] is the causal agent of scald in barley (Hordeum�ulgare L.), a serious disease which occurs in all ofmajor barley growing regions of the world. It cancause considerable reductions in yield and quality ofthe grain. Yield loss estimates as high as 35–40 %have been reported (JAMES et al. 1968) and between7 and 28 % in Norway (SALAMATI 1997). Therefore,understanding the disease is of high priority. However,genetic analysis of the host–pathogen interactions ofthe barley–scald pathosystem is difficult. Geneticanalyses of host and pathogen have been hamperedby the lack of a universally recognized set of differen-tials, each with a single resistance gene and free ofproblems with respect to synonyms as to genotypesor loci. Numerous reports indicate that R. secalisisolated from barley exhibits a high degree of patho-genic variability (HANSEN and MAGNUS 1973; JACK-

SON and WEBSTER 1976; CEOLONI 1980; TEKAUZ

1991; SALAMATI and TRONSMO 1997). The use ofsmall test plant populations and/or single isolates ofR. secalis have frequently made it impossible to verifywhether the genes in two resistant genotypes wereallelic, identical or closely linked. As a result of thesefactors, the actual genetic diversity of the host resis-tance, and hence the potentially available resistance

sources for breeding purposes is equivocal. It is in-dicative that the last major comprehensive study ofscald resistance genetics was carried out by HAB-

GOOD and HAYES (1971). Further, some of the differ-ential varieties used to differentiate R. secalispathotypes have more than one resistance gene, andsome resistance genes may be shared among two ormore differentials (GOODWIN 1988). This can beovercome by means of near-isogenic lines (NILs).

In many crop species sets of NILs are now avail-able. NILs with different specific resistance genes,which are useful for studies of host–parasite interac-tions, have been developed in oats (FREY et al. 1971),wheat (BRIGGLE 1969) and barley (KøLSTER et al.1986; HINZE et al. 1991). The latter paper used one ofthe numerous sets that J. Mac Key has developed forvarious diseases in wheat, oats and barley. In theHINZE et al. (1991) case, 8 NILs in cultivar ‘Ingrid’ asthe recurrent parent (RP) were used to target theml-o resistance locus in barley. In the NIL pro-gramme reported here, J. Mac Key at its inception in1977 started with 23 donors (Table 1) carrying knownor unknown genes for scald resistance. Strict back-crossing was performed in the cultivar ‘Ingrid’ as RP.Various problems have arisen during this long pro-cess: variable testing conditions, different resistance

Resistance to scald in barley 187Hereditas 137 (2002)

Table 1. O�er�iew of the 23 culti�ars of known and reported sources of scald resistance in barley used in NILde�elopment and their status

Reference ResistantCultivar TestGene designationsNIL status isolates

BAKER and LARTER 1963 BC7F10*‘Abyssinian’ (CI 668) 4004Rh9None GRO�NNERO�D et al. 2002Rrs1Abyssinian BJO�RNSTAD et al. 2002

RIDDLE and SUNESON 1948 BC4F8Unknown 2‘Abyssinian’ (CI 1233)Rh2, 3‘Atlas 46’ (CI 7323) DYCK and SCHALLER 1961a,b BC7F6* 4004UnknownBenton (CI 1227) SCHALLER et al. 1963 BC3F5 2

HABGOOD and HAYES 1971 BC7F10*Rh1, rh6 4004‘Brier’ (CI 7157)BJO�RNSTAD et al. 2002Rrs1Brier

SCHALLER et al. 1963 BC7F6Unknown 2CI 1237UnknownCI 2230 SCHALLER et al. 1963 BC7F2 2

HABGOOD and HAYES 1971 BC4F3 4004CI 4364 rh11STARLING et al. 1963 BC7F6Unknown 2CI 6168

Rh3, 6CI 8162 HABGOOD and HAYES 1971 BC7F11* 4004Rrs1Brier BJO�RNSTAD et al. 2002

This publication BC7F11*Unknown 4004‘Hispont’ (CI 8828)Rh1‘Hudson’ (CI 8067) HABGOOD and HAYES 1971 BC7F11* 4004rh5, 6Jet (967) BAKER and LARTER 1963 BC7F3 4004

BJO�RNSTAD et al. 2002rrs1Jet

HABGOOD and HAYES 1971‘La Mesita’ (CI 7565) BC7F9* 4004Rh4, 10BJO�RNSTAD et al. 2002Rrs1La Mesita

Rh2, rh6‘Modoc’ (CI 7566) HABGOOD and HAYES 1971 BC7F11* 4004BJO�RNSTAD et al. 2002Rrs1Modoc

WELLS and SKOROPAD 1963 BC6F4rh8 4004Nigrinudum (CI 2222)Rrs2CI 2222 BJO�RNSTAD et al. 2002rrsx (rhx)Nigrinudum (CI 11549) PATIL 2001 BC2F11 4004

BJO�RNSTAD et al. 2002Rrs4CI 11549Rh1, 6, 7Osiris (CI 1622) DYCK and SCHALLER 1961a,b BC2F2 4004Rh10Pioneer (CI 9508) HANSEN and MAGNUS 1973 BC3F4 4004

http://www.ars-grin.go�/cgi-bin/Quinn (CI 1024) BC6F5Unknown 2npgs/html/acchtml.pl?1104769BAKER and LARTER 1963 BC7F11Steudelli (CI 2226) 4004rh6, 7BJO�RNSTAD et al. 2002Rrs1Steudelli

Rh4Trebi (CI 936) DYCK and SCHALLER 1961a BC2F5 4004HABGOOD and HAYES 1971 BC7F7* 4004‘Turk’ (CI 14400) Rh5, rh6BJO�RNSTAD et al. 2002Rrs1Turk

* NILs used in the present study.

levels, escapes, loss or decay and replacement ofisolates, donors with susceptible synonyms, etc. havesometimes made it necessary to revert to earlier BCgenerations. In 1996 the whole programme wasscreened with isolate ‘4004’, which is avirulent to 21of the 23 sources. Later this isolate was supplementedwith isolate ‘2’, which was avirulent to the remainingtwo but virulent to several others. The BC progenieswere screened with these isolates 1996.

Currently most available NILs have been devel-oped by backcrossing a gene of interest to a RPhaving otherwise desirable properties. The residualdonor material that segregates independently of theselected gene is expected to decline by one-half ineach generation. The theoretical rate of recovery (in%) of the RP is [1− (0.5)n+1]×100, where n equalsthe number of backcross (BC) generations, plus a

final selfing generation. According to this equation,the NILs in our study should produce a progenycontaining about 99.9 % of the RP genome, as theyare in BC7 generation. However, the segment of thechromosome containing the selected gene is reducedat a much slower rate, a phenomenon termed ‘linkagedrag’ (BRINKMAN and FREY 1977; STAM and ZEVEN

1981). This can be a problem for the expression ofthe selected allele in the desired background. How-ever, it is also possible to exploit the linkage drag offavourable associations of genes adjacent to a markerlocus. The marker locus can tag the genomic segmentand assist its manipulation in a breeding program.

In a study of the most promising NILs, BJO�RN-

STAD et al. (2002) reported 96 % RP-NIL averagesimilarity, and the marker differences on chromo-somes 3H and 7H corresponded to known scald

V. Patil et al.188 Hereditas 137 (2002)

resistance loci. In the current study the 9 most ad-vanced NILs, parents, F1 and F2 progenies werestudied in NIL by NIL half-diallel design, in order tounderstand the allelism/identity of the NILs anddominance or recessiveness.

MATERIAL AND METHODS

Donors and NILs

In 1996–98 several comprehensive tests identifiedBC7 lines at different stages from most donors. How-ever, only 9 BC7 lines were ready to be selected forthe present study; ‘CI 668’ (‘Abyssinian’), ‘CI 7323’(‘Atlas 46’), ‘CI 7157’ (‘Brier’), ‘CI 8162’, ‘CI 8828’(‘Hispont’), ‘CI 8067’ (‘Hudson’), ‘CI 7565’ (‘LaMesita’), ‘CI 7566’ (‘Modoc’) and ‘CI 4400’ (‘Turk’)(Table 1).

Isolates used

The R. secalis, isolate ‘4004’(syn. ‘103’) of Danishorigin (JøRGENSEN 1992) was used in June 2000 andisolate ‘2’ (SALAMATI and TRONSMO 1997) used inDec. 2000–Jan. 2001. In fact, the second test wasintended to be a replication of the first, but isolate‘4004’ had become contaminated with isolate ‘2’.Since isolate ‘2’ has 3–4 times faster in vitro growthrate and is much more virulent, the effective inocu-lum was isolate ‘2’, when compared with previousexperience.

NIL×NIL

A complete NIL×NIL half-diallel series was pro-duced between the 9 NILs resulting in 36 families.The crosses are listed in Table 2. Individual F1 plantswere raised for F2 seeds, and each plant was har-vested separately and kept to check for possibleselfings.

Experimental design

The plants were grown in Jiffy strips, in 30×20 cmplastic trays with 55 strip units in each tray and withthree plants in each unit. The experiment conductedin May–June 2000 in a randomized complete blockdesign, with 36 crosses and 3 replications. A total of27 trays was used, with 9 trays in each replication. Inturn, each tray had 4 blocks, each of which consti-tuted a cross. Therefore, all the 36 crosses wereincluded in a replication. While crosses were random-ized within replications, within crosses the design wasfixed with a total of 13 entries: ‘Ingrid’ as the suscep-tible control, each of the donors and their NILs, oneF1 and 7 F2s, each representing progenies from adifferent F1 plant. Three extra ‘strips’ of ‘Ingrid’ weresown per tray as additional controls. In the Dec.

Table 2. List of crosses in�ol�ed in NIL×NIL halfdiallel design

Cross No. NIL×NIL cross

1 ‘Turk’-NILבBrier’-NIL2 ‘Turk’-NILבCI 8162’-NIL

‘Turk’-NILבLa Mesita’-NIL34 ‘Turk’-NILבHispont’-NIL5 ‘Turk’-NILבAtlas 46’-NIL6 ‘Turk’-NILבModoc’-NIL7 ‘Turk’-NILבHudson’-NIL8 ‘Turk’-NILבAbyssinian’-NIL9 ‘Brier’-NILבCI 8162’-NIL

10 ‘Brier’-NILבLa Mesita’-NIL11 ‘Brier’-NILבHispont’-NIL

‘Brier’-NILבAtlas 46’-NIL1213 ‘Brier’-NILבModoc’-NIL14 ‘Brier’-NILבHudson’-NIL

‘Brier’-NILבAbyssinian’-NIL1516 ’CI 8162’-NILבLa Mesita’-NIL17 ‘CI 8162’-NILבHispont’-NIL18 ‘CI 8162’-NILבAtlas 46’-NIL19 ‘CI 8162’-NILבModoc’-NIL20 ‘CI 8162’-NILבHudson’-NIL

‘CI 8162’-NILבAbyssinian’-NIL2122 ‘La Mesita’-NILבHispont’-NIL23 ‘La Mesita’-NILבAtlas 46’-NIL24 ‘La Mesita’-NILבModoc’-NIL25 ‘La Mesita’-NILבHudson’-NIL26 ‘La Mesita’-NILבAbyssinian’-NIL27 ‘Hispont’-NILבAtlas 46’-NIL28 ‘Hispont’-NILבModoc’-NIL

‘Hispont’-NILבHudson’-NIL29‘Hispont’-NILבAbyssinian’-NIL30

31 ‘Atlas 46’-NILבModoc’-NIL32 ‘Atlas 46’-NILבHudson’-NIL33 ‘Atlas 46’- NILבAbyssinian’-NIL34 ‘Modoc’-NILבHudson’-NIL35 ‘Modoc’-NILבAbyssinian’-NIL36 ‘Hudson’-NILבAbyssinian’-NIL

2000–Jan. 2001 test a similar design was followedwith only two replications.

Growth conditions and scoring of symptoms

The plants were grown at 16–18°C throughout thetest period either in air-conditioned day light growthchamber during May–June 2000, or in a greenhouseduring Dec. 2000–Jan. 2001. Inocula were made asdescribed by SALAMATI and TRONSMO (1997). Thespraying, scoring scale and disease rating was asdescribed by REITAN et al. (2002). The plants werescored individually but means of the three plants,means of replicates and means of tests were consid-ered for statistical analyses.

Statistical methods

Results from inoculation by each isolate were treatedseparately, due to strong interactions between geno-

Resistance to scald in barley 189Hereditas 137 (2002)

types and isolates. Average differences betweencrosses (fixed) and replicates (random effects) for‘Ingrid’, F1, F2 and their differences were analysed bytwo-way ANOVA. Differences between donors andcorresponding NILs (pairwise) were computed fromall the crosses where they were analysed by one-wayANOVA. The F1 resulting from NIL×NIL crosseswas subjected to diallel analysis. The GARDNER andEBERHART (1966) analysis II was employed to parti-tion the total variance and estimate GCA, SCA andaverage heterosis. The Hayman and Jinks’ analysis(JINKS and HAYMAN 1953) was used to plot theWr–Vr (covariance–variance) graph to determine thetype of gene action. The distribution of NILs alongthe regression slope was determined and the NILswith the relatively most dominant or recessive genesidentified. The F2 plants were grouped into classes;‘Resistant’ (R), ‘Moderately Resistant’ (MR), ‘Mod-erately Susceptible’ (MS) and ‘Suseptible’ (S) depend-ing on their scores to simpler identify the segregatingcrosses. Standard errors (SE) were calculated bypooling the results of the three replicates. Differencesbetween entries within crosses was tested by t-testsusing the respective SE’s. All the data was analysedby the statistical program NM (Nissen, AgriculturalUniversity of Norway 2000, unpubl.).

RESULTS

General features of the inoculation tests

In the May–June 2000 test there were scatteredmildew infections, in particular in one half of replica-

tion 3. However, this was not a serious problem as wecould differentiate discolouring due to mildew orscald. The inoculation conditions in the Dec. 2000–Jan. 2001 test were fairly good, generally ‘Ingrid’ hada variable reaction and a ‘MS’ type, the donors;‘Turk’, ‘Brier’ and ‘CI 8162’ were ‘S’. The results ofDec.–Jan. 2001 test corresponded well with previoustests with isolate ‘2’. The most probable effect ofadmixture may have been a somewhat diluted inocu-lum and we consider the test quite informative as tothe types of gene action (dominance/recessiveness)involved.

The levels of precision of the tests were analysed bytwo way ANOVA of the different entries in eachcross. From Table 3a, it can be seen that with respectto ‘Ingrid’ and ‘4004’, no average replicate effectswere detected, but there were significant differencesbetween ‘Ingrid’ in the different crosses. This may beascribed to weaker inoculation in parts of replicate 3(see below). With isolate ‘2’, no such effects weredetected. The means of F1 and F2s differed signifi-cantly between crosses, as expected. There were noeffects of replications, except for the mean of F2s for‘4004’, probably due to segregating crosses. In asample of 21 plants, susceptible and resistant proge-nies may have been present in different ratios in thedifferent replicates. In the case of isolate ‘2’, no sucheffects were detected, maybe due to a narrower phe-notypic range. However, weak replication effectswere detected for F1’s, the reasons for which areobscure. Thus the overall precision of the tests werequite good.

Table 3a. Two-way ANOVA of pooled results across replications and crosses for the two isolates of Rhynchospo-rium secalis

Source Isolate ‘4004’ Isolate ‘2’

df F P valuesFdf P values

2‘Ingrid’ between replications 0.1 1ns 0.12 ns0.024*1.78between crosses 0.331.1535 35

3.052F� 1 between replications 5.0710.52 0.029*3.28 �0.0001*** 35 2.15 0.013*between crosses 356.45F� 2 between replications 0.003** 1 1.59 0.2123.81 �0.0001*** 35between crosses 4.27 �0.0001***35

Table 3b. One-way ANOVA across the donors and their NILs

Isolate ‘2’Source Isolate ‘4004’

F P values df F P valuesdf

Donors 8 10.50 �0.0001*** 8 56.97 �0.0001***�0.0001***27.228�0.0001***10.558NILs

NIL–Donor 8 5.50 �0.0001*** 8 11.87 �0.0001***

V. Patil et al.190 Hereditas 137 (2002)

From Table 3b, it can be seen that there werehighly significant differences between the donors,NILs and also the difference between NILs anddonors, irrespective of the isolates.

Isolate ‘4004’

The mean scores with SE and the ranges of ‘Ingrid’,donors and NILs are presented in Table 4, while therange and segregation status for F2s are presented inTable 5. Similarly Table 6 gives the mean scores withSE for F1, average heterosis, better parent heterosisand the mean differences of NILs and donors. ‘In-grid’ was ‘S’ with a mean score of 4.7�0.1 (Table 4),but the range was variable as there was relatively lesssevere infection due to less humid conditions in onehalf of replication 3, causing occasional ‘R’ or ‘MR’phenotypes in ‘Ingrid’ in crosses 7 and 26. All the 9 %of ‘Ingrid’ plants that were ‘R’ type, were fromreplication 3, and only 2 % had scores from 1.0 to2.0. This could be attributed to the mentioned inocu-lation conditions and possibly also some inducedresistance due to an infection with mildew. Toconfirm the precision, we checked the mean scores foreach of the replications and later subjected ‘Ingrid’ toANOVA by including only the first two replications.There were no significant effects either between repli-cations or between crosses. This suggested that theoccasional ‘MS’ scores of ‘Ingrid’ in these crosses didnot affect the overall precision of the tests.

In general, the donors were either ‘R’ or ‘MR’type; ‘Turk’ (0.7�0.1) was ‘R’ while ‘Modoc’ (2.1�

0.2) was ‘MR’. The ranges and SEs show that ‘LaMesita’, ‘Modoc’ and ‘Abyssinian’ were the mostvariable (Table 4).

‘Turk’-NIL (1.0�0.1) was ‘R’ while ‘Abyssinian’-NIL (2.7�0.1) was a weak ‘MR’. Further, ‘Modoc’-NIL (SE�0.3) was the most variable NIL followedby ‘Atlas 46’-NIL (SE�0.2) (Table 4). These detailscan be confirmed by the corresponding individualSE’s in the results of PATIL (2001). In most cases thedonors were more resistant than the NILs, with theexception of ‘Brier’-NIL, which tended to be betterthan the donor (Table 4).

Isolate ‘2’

‘Ingrid’ was ‘MS’ with a mean score of 3.4�0.1(Table 4). There was a wider spectrum of reactionsamong donors, ranging from ‘Hispont’ (0.9�0.2)and ‘Atlas 46’ (1.0�0.1), to ‘Brier’ (4.9�0.1), CI8162 (4.8�0.1) and ‘Turk’ (4.6�0.3), but more nar-row among NILs. It can also be noted that ‘Modoc’and ‘Hudson’ (SE�0.3) were the most variable(Table 4). Most NILs showed a better resistancereaction than the donors, with the exception of the‘Hispont’-NIL and ‘Atlas 46’-NIL. For example,there was a significant difference between ‘CI 8162’and ‘CI 8162’-NIL (‘S’ vs ‘MR’). Correspondingly,‘La Mesita’-NIL (1.1�0.2) and ‘Abyssinian’-NIL(1.3�0.1) were ‘R’ types, while ‘La Mesita’ (2.1�0.2) and ‘Abyssinian’ (2.7�0.2) were ‘MR’ types. Itcan be observed from Table 4, that the NILs of‘Turk’, ‘Brier’, ‘CI 8162’, ‘La Mesita’, ‘Atlas 46’,

Table 4. Reaction of the donors and their NILs against the two isolates of Rhynchosporium secalis. Pooled meanscores �SE and the ranges are gi�en

Donors/NIL Isolate ‘4004’ Isolate ‘2’

Mean score�SE Range nMean score�SEnRange

‘Ingrid’ 4.7�0.1 1–5 300 3.4�0.1 2–4 210444–54.6�0.2650–20.7�0.1‘Turk’

3.0�0.2680–21.2�0.1 46‘Turk’-NIL 2–41.5�0.1 0–2.5 70 4.9�0.1 4–5‘Brier’ 461.4�0.1‘Brier’-NIL 0–2.5 72 3.2�0.2 2–4 421.6�0.1’CI 8162’ 0–3 66 4.8�0.1 3–5 41

391–42.8�0.2641–42.2�0.1’CI 8162’-NIL1.6�0.2‘La Mesita’ 0–3.5 67 2.1�0.2 0–3 45

‘La Mesita’-NIL 1.6�0.1 1–3 72 1.1�0.2 0–3 47460–30.9�0.2720–31.4�0.1‘Hispont’

‘Hispont’-NIL 1.4�0.1 0–3 66 0.9�0.1 0–2.5 410.9�0.1 0–2.5 71‘Atlas 46’ 1.0�0.1 0–2 42

‘Atlas 46’-NIL 1.8�0.2 0–3 70 1.6�0.2 0–3 42‘Modoc’ 2.1�0.2 0–4 65 3.1�0.3 1–4 42‘Modoc’-NIL 2.4�0.3 1–5 68 1.5�0.2 0–3 41

351–42.7�0.362‘Hudson’ 0–20.9�0.1‘Hudson’-NIL 2.0�0.1 1–3.5 63 1.6�0.2 1–3 32‘Abyssinian’ 1.7�0.1 0–4 70 2.7�0.2 1–4 38‘Abyssinian’-NIL 2.6�0.1 0–5 55 1.3�0.1 0–2 40

Resistance to scald in barley 191Hereditas 137 (2002)

Table 5. Range and segregation of NIL×NIL F2 progenies when challenged with the two isolates of Rhynchospo-rium secalis

Cross No. Isolate 4004 Isolate 2

n Segregates F2 range n Tentative segregatesF2 range

60 No 1–41 41 –0–20–2.5 63 No 1–4 42 –2

623 No 1–4 40 No0–260 No 0–31–2.5 39 No4

0–45 58 Yes 1–4 39 No58 No 1–4 386 –1–361 Yes 1–41–5 427 –

1–48 62 No 0–4 40 –58 No 1–4 38 No9 0–460 No 1–40–2.5 4010 No59 No 0–4 4211 No1–2.561 Yes 1–40–5 40 –12

1–313 55 No 1–4 34 –60 Yes 1–41–5 3714 No

1–415 55 No 0–3.5 33 –1–416 62 No 0–4 40 No

59 No 0–40.5–2 40 –170–518 63 Yes 1–4 41 –

60 No 1–4 4119 No0.5–356 Yes 0–40–5 3820 –

1–521 43 No 1–4 40 –60 No22 0–2 42 No0–2.562 Yes 1–51–5 40 Yes2358 No 0–2 4124 No1–558 Yes 0–30–5 37 No25

1–526 62 No 0–2.5 42 No61 Yes 0–30.5–5 4227 No

0.5–328 58 No 0–2 39 No1–529 61 Yes 0–3 41 No

62 No 0–31–4 40 No300–531 59 Yes 0–3 28 No

61 Yes 0–3 3732 No1–558 No 0–30–5 4033 No

1–534 62 Yes 0–3 21 –6335 No 1–2 41 –1–558 No 1–3 38 –1–536

Table 6. Results of the ANOVA of the diallel cross

Source Isolate ‘4004’ Isolate ‘2’

F P values df F P valuesdf

3.72 0.027* 1Replications 7.04 0.01*244 3.39 �0.0001*** 44 2.35 0.003**Treatments

8NILs 3.79 0.001** 8 2.98 0.009**3.25 �0.0001*** 3535 2.26 0.006**Crosses

1Average heterosis 5.14 0.024* 1 0.71 –6.55 �0.0001*** 8GCA 5.26 0.0002***82.27 0.0025** 2727 1.37SCA 0.17

V. Patil et al.192 Hereditas 137 (2002)

‘Modoc’ and ‘Hudson’ were slightly more variable(SE�0.2).

Assessment of resistance in the F1 and F2 generations

a. Gene action

Isolate ‘4004’.

The results of ANOVA of the diallel analysis (Table6) show that there were significant effects for replica-tions, treatments, NILs, crosses, average heterosis,general combining ability (GCA) and specificcombining ability (SCA). The diallel analysis meansof the 9 NILs in hybrids combination (bold figures indiagonal corresponds to NIL means in Table 4),average heterosis and GCA for individual NILs arepresented in Table 7. The SCA was lower than GCA(Table 6) as certain NILs did not combine well (Table7, e.g. ‘CI 8162’-NIL× ‘Modoc’-NIL and ‘LaMesita’-NIL× ‘Modoc’-NIL). ‘Turk’-NIL was themost resistant followed by ‘La Mesita’-NIL, ‘His-pont’-NIL and ‘Brier’-NIL. Interestingly ‘La Mesita’-NIL and ‘Hispont’-NIL displayed high and similarresistance, while ‘Modoc’-NIL and ‘Abyssinian’-NILwere also similar, but less resistant. The diallel analy-sis of the F2 means were consistent with these results(PATIL 2001).

A detailed analysis of F1 and parental means waspresented by PATIL (2001). In general the averageheterosis was slightly negative indicating increasedresistance. However, few of the crosses showed sig-nificant differences (p=0.024 in Table 3a). Also thebetter parent heterosis showed only insignificant ef-fects. This corresponded well to the much strongerGCA than SCA effects, indicating predominantlyadditive gene action but with dominance present incertain cross combinations.

The Wr-Vr graph (Fig. 1a) gives a visual interpre-tation of genetic effects of the individual NILs. Itindicates that ‘Atlas46’-NIL, ‘Brier’-NIL, ‘Turk’-NIL, ‘Hudson’-NIL and ‘Hispont’-NIL had domi-nant genes while ‘CI 8162’-NIL, ‘Modoc’-NIL,‘Abyssinian’-NIL and ‘La Mesita’-NIL had recessivegenes for scald resistance. The Wr-Vr graph of the F2

means conformed qualitatively to these results butdifferences in Vr and Wr were less marked. ‘CI8162’-NIL, was located closer to the origin than inthe F1 (PATIL 2001).

Isolate ‘2’

There were significant effects for replications, treat-ments, NILs, crosses, and GCA but not for averageheterosis and SCA (Table 6). The most importantresult compared with the other isolate was the stronginteraction with regard to resistance, as well as the T

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Resistance to scald in barley 193Hereditas 137 (2002)

Fig. 1a–b. a) Relationship between Wr–Vr for R. secalisisolate ‘4004’ in NIL×NIL diallel. b) Relationship betweenWr–Vr for R. secalis isolate ‘2’ in NIL×NIL diallel.

showed that the crosses between consistently ‘R’ typeNILs produced F2 progenies which were of the sameclass. From Table 5 it can be observed that 13 of thecrosses segregated in the F2 generation. A commonfeature for all these crosses with segregating F2 pro-genies was that they involved either ‘Atlas 46’-NIL or‘Hudson’-NIL as one of the parents. There wereother crosses which produced susceptible progeniesbut they were not considered as segregating as theirresponses were within the parental range (crosses 8, 9,15, 16, 21, 24, 26, 30, 33, 35 and 36).

Isolate ‘2’

The interpretation of these data is more difficult incomparison with the other isolate. As before, onlysusceptible segregants from ‘R’× ‘R’ crosses wereindicative. However segregants lacking the resistancein both NILs will be ‘MS’ type like ‘Ingrid’. In manycases an occasional ‘MS’ type occurred in theparental NILs (Table 5). However, some clear casesdid occur, like cross 23 involving ‘Atlas 46’-NIL.Moreover, crosses 28 and 35 clearly did not segre-gate, indicating allelism. In short, this isolate was lessinformative as compared to the segregation in theisolate ‘4004’.

DISCUSSION

Assessment of experimental precision

We did not randomise within crosses due to theinconvenience and risk of errors in sowing. This lackof randomisation does represent a problem for thediallel analysis, since the NIL1, NIL2 and F1 entrieswere confounded within each cross and this maycontribute to some environmental covariance, which,although it can be checked by the replications, is alimitation in the statistical analyses. We used theGARDNER and EBERHART (1966) analysis for esti-mating the combining ability, as the parents wereNILs. The rather low regression coefficients in theWr–Vr graphs indicate the failure of some of theassumptions for this analysis, either non-independentgene distribution among the parents or gene interac-tion (epistasis) (CHRISTIE and SHATTUCK 1992). Webelieve that the most reasonable explanation is theformer, given the indications that 7 of the linesmultiple alleles at the Rrs1 complex (BJO�RNSTAD etal. 2002). Indications of gene interaction would onlybe detectable with isolate ‘2’, due to the weak resis-tance factor in ‘Ingrid’. However, this gene (locatedon chromosome 7H, on the same arm as Rrs2) wouldbe fixed in most lines, except possibly the ‘Atlas46’-NIL. PATIL (2001) found very little to support anyepistasis in crosses with this NIL.

reversal of dominance. The Wr–Vr graph (Fig. 1b)shows that the genes in ‘Modoc’-NIL, ‘Hispont’-NIL,‘Abyssinian’-NIL and ‘Atlas 46’-NIL showed moredominant gene action, while ‘Turk’-NIL and ‘Brier’-NIL were recessive.

The resistance in F1 was either increased or wasequal to the best parent, but in crosses 35 and 36 itwas reduced (PATIL 2001). There were two othercrosses (29 and 31) where the F1 was not better butthey were highly variable and not significant. Theaverage heterosis in crosses 4, 6, 10, 11, 15, 19, 20and 27 showed increased resistance.

Range and segregation

Isolate ‘4004’

The range and segregation status of the F2 progeniesare given in Table 5. Only crosses between resistant(‘R’ or ‘MR’) NILs producing susceptible F2 proge-nies (outside the parental range) were considered toindicate resistance on different chromosomes. Whencompared to the parental ranges (Table 4), the results

V. Patil et al.194 Hereditas 137 (2002)

Isolate ‘4004’

The response of all the donors (except ‘Hispont’) inthe present study were in agreement with earlierreports (JøRGENSEN 1992; REITAN et al. 2002). Theresponse of ‘Hispont’ was also consistent with previ-ous results (BJO�RNSTAD, unpubl.). The response ofthe NILs was consistent with the donors. The NILsfrom ‘R’ type donors were either ‘R’ or ‘MR’ typewhile the NILs from ‘MR’ type donors were ingeneral ‘MR’.

Isolate ‘2’

‘Ingrid’ showed ‘MR’– ‘MS’ phenotype as previouslyreported by GRO�NNERO�D et al. (2002) andBJO�RNSTAD et al. (2002). The disease infection wasmore severe on six of the donors and they were ‘S’types (Table 4), the exceptions being ‘Atlas 46’, ‘His-pont’ and ‘La Mesita’. Similar responses in ‘Atlas 46’,‘CI 8162’ and ‘Turk’ were reported by REITAN et al.(2002). In contrast, SALAMATI and TRONSMO (1997)reported that this isolate infected 86 % of the differen-tials used and ‘La Mesita’ was completely susceptible.Similarly GRO�NNERO�D et al. (2002) report that‘Abyssinian’ had a less resistant reaction than ‘In-grid’, which was not the case in our study. The NILsexhibited a stronger resistance compared to thedonors and RP, there was transgression in seven ofthe donors (Table 4). This transgression can be ex-plained by the Rrs12Ingrid resistance allele from the RP(GRO�NNERO�D et al. 2002) and BJO�RNSTAD et al.(2002). In general this is one of the most virulentisolates and thus a useful supplement to isolate ‘4004’.

Segregation in F2

The results show that crosses between 7 and 9 NILparents generally produced F2 populations which didnot segregate indicating that the genes for scald resis-tance in the two parents are either allelic or closelylinked on the same chromosome (HABGOOD andHAYES 1971). The F2 progenies segregated in crossesinvolving either ‘Atlas 46’-NIL or ‘Hudson’-NIL asone of the parents with isolate ‘4004’ (Table 5),indicating that the genes for scald resistance are ondifferent chromosomes. With isolate ‘2’, the data wasless informative, given the resistance in ‘Ingrid’ result-ing in a reduced range of disease reactions.

Analyses of indi�idual donor/NIL-pair

In the paper by BJO�RNSTAD et al. (2002) changes inthe nomenclature of R. secalis resistance have beenmade based on the marker and phenotypic analy-sis. In this paper we look at inoculation data withthe two isolates (‘4004’ and ‘2’) for each pair indetail.

‘Turk’– ‘Turk’-NIL

According to DYCK and SCHALLER (1961a,b), ‘Turk’was found to be controlled by two dominant genes(Rh3 and Rh5), while BAKER and LARTER (1963)suggested that it had a single gene (Rh3) with com-plete dominance. This was later supported by thereport of STARLING et al. (1971). However, HAB-

GOOD and HAYES (1971) reported that it had adominant (Rh1) and a recessive gene (rh6). The com-mon feature for all these studies is that the ‘Turk’ hadCI (Cereal Inventory) number of 5611-2, while the‘Turk’ we used in our study was ‘CI 14400’.

The donor ‘Turk’ and its NIL was ‘R’ to the isolate‘4004’. As expected, all the F1s involving ‘Turk’-NILwere ‘R’. In contrast both the donor and the NILwere ‘S’ with the isolate ‘2’ (Table 4), most of the F1swere ‘R’ type, the exceptions being cross 3 (Table 6).A similar reaction of the donor with these two isolateshas been reported by REITAN et al. (2002). Thesusceptibility of the F1 in cross 3 with isolate ‘2’ mightbe attributed to an occasional selfing in NIL1. Ourresults indicates that ‘Turk’ has a dominant gene(Rrs1Turk) previously ascribed to chromosome 3H,this gene was successfully introgressed into ‘Turk’-NIL. The marker pattern confirmed these results(BJO�RNSTAD et al. 2002). The Wr–Vr graphs furtherconfirmed the dominant gene action of ‘Turk’ allelewith isolate ‘4004’ (Fig. 1a), while with isolate ‘2’ theallele behaved recessively (Fig. 1b). However,BJO�RNSTAD et al. (2002), did not trace the rh6 genepreviously ascribed to chromosome 4H, based on thescreening of the available microsatellites on this chro-mosome.

‘Brier’– ‘Brier’-NIL

A single dominant gene was responsible for scaldresistance in ‘Brier’ (DYCK and SCHALLER 1961a,b),while HABGOOD and HAYES (1971) suggested thatthere were two genes (Rh and rh6). The results ofBJO�RNSTAD et al. (2002) and our study indicates asingle locus (Rrs1Brier) on chromosome 3H. We didnot find any trace of the rh6 gene.

The donor ‘Brier’ and its NIL were ‘R’ to theisolate ‘4004’, while with the isolate ‘2’, the donor isa ‘S’ and the NIL ‘MS’ (Table 4). This improvementof the NILs as compared to the donors can beattributed to the resistance allele in the RP. TheWr–Vr graph show that ‘Brier’-NIL had dominantgene action when tested with isolate ‘4004’ (Fig. 1a),while in the case of isolate ‘2’ it behaved recessively(Fig. 1b).

‘CI 8162’– ‘CI 8162’-NIL

According to HABGOOD and HAYES (1971), this linehas a single incompletely dominant gene (Rh3) at the

Resistance to scald in barley 195Hereditas 137 (2002)

Rh complex locus on chromosome 3H. This gene hasbeen transposed to an allele at the Rrs locus, andreferred as Rrs1CI 8162 by BJO�RNSTAD et al. (2002).

The donor ‘CI 8162’ was ‘R’ while the NIL in-clined more towards ‘MR’ reaction to the isolate‘4004’. With isolate ‘2’ the donor was ‘S’ and the NILa ‘MR’– ‘MS’ type (Table 4), due to the resistanceallele in RP seem to contribute to the increasedresistance in NILs. REITAN et al. (2002) also reportedthat ‘CI 8162’ was resistant to isolate ‘4004’ butsusceptible to isolate ‘2’. The F2 segregation (Table 5)and Wr–Vr graph (Fig. 1a) with ‘4004’ indicated thatthe donor and its NILs had a recessive allele onchromosome 3H. However, the Wr–Vr graph withisolate ‘2’ (Fig. 1b) indicates that ‘CI 8162’-NILalleles act incompletely dominant.

‘La Mesita’– ‘La Mesita’-NIL

The Rh4 gene was responsible for resistance in ‘LaMesita’ (DYCK and SCHALLER 1961a). A later studyby HABGOOD and HAYES (1971) reported that therewere two genes, an incompletely dominant gene Rh4

and a dominant gene Rh10 involved in conferringresistance against scald. The Rh4 locus has beenupdated as Rrs1La Mesita by BJO�RNSTAD et al. (2002).No other dominant gene was detected.

The donor ‘La Mesita’ and its NIL were ‘R’ withboth the isolates (Table 4). The F2 progenies segre-gated in crosses 23 and 25 with ‘4004’ and only incross 23 with isolate ‘2’, both pointing to chromo-some 3H as the location. Contrary to our resultsSALAMATI and TRONSMO (1997) reported that donorwas fully susceptible to isolate ‘2’. The allele in ‘LaMesita’-NIL acted incompletely dominant to the iso-late ‘4004’ (Fig. 1a), while with isolate ‘2’, it behavedrecessively (Fig. 1b), due to ‘MR’ reaction in cross 3(Table 6 and 8).

‘Hispont’– ‘Hispont’-NIL

The ‘Hispont’ allele has an unclear origin and noprior information is available. Both the donor and‘Hispont’-NIL were ‘R’ to the two isolates (Table 4).These results are consistent with previous results(BJO�RNSTAD, unpubl.). The F2 progenies segregatedin the crosses 27 and 29 when tested with isolate‘4004’ (Table 5), indicating that the resistance is dueto an allele at the Rrs/Rh locus. ‘Hispont’-NIL and‘La Mesita’-NIL were identical in reaction to isolate‘4004’ (Table 6). A similar pattern was also observedin studies with molecular markers (BJO�RNSTAD et al.2002), indicating identity problems of the two NILs.In the Wr–Vr graph (Fig. 1a) both the NILs wereincompletely dominant, where as they appeared moredifferent when tested with isolate ‘2’ (Fig. 1b; ‘His-pont’-NIL dominant and ‘La Mesita’-NIL recessive).

‘Atlas 46’– ‘Atlas 46’-NIL

HABGOOD and HAYES (1971) reported that ‘Atlas 46’has two dominant genes, Rh1 and Rh2. The Rh1 genefrom ‘Turk’ (‘CI 5611-2’) was originally introgressedinto the genetic background of ‘Atlas’ (HABGOOD

and HAYES 1971). BJO�RNSTAD et al. (2002) detectedmarkers on 7H in the region of Rrs2 (SCHWEIZER etal. 1995) and RP alleles in the Rrs1 region.

‘Atlas 46’ and its NIL were ‘R’ to both the isolates(Table 4), in accordance with REITAN et al. (2002).The Wr–Vr graph for both isolates (Fig. 1a,b) indi-cated that ‘Atlas 46’-NIL has a dominant allele on achromosome other than 3H, as the F2 progeniesinvolving ‘Atlas 46’-NIL as a parent segregated in 7crosses with isolate ‘4004’ and a single cross with ‘2’(Table 5). Hence it carries the Rrs2Atlas gene.

‘Modoc’– ‘Modoc’-NIL

According to HABGOOD and HAYES (1971), there is adominant gene Rh2 at the Rh locus on chromosome3H and another gene rh6 at a different locus respon-sible for resistance in ‘Modoc’. BJO�RNSTAD et al.(2002) have designated the former locus as Rrs1Modoc.

The donor and ‘Modoc’-NIL were ‘MR’ to isolate‘4004’, while the donor was ‘S’ and the NIL ‘R’ toisolate ‘2’ (Table 4). There was segregation in a singlecross with isolate ‘4004’ (Table 5). ‘Modoc’-NIL hadalleles that act recessively when tested with ‘4004’(Fig. 1a). In contrast, the results of diallel anlysis(Table 6) and Wr–Vr graph (Fig. 1b) indicate that‘Modoc’-NIL had a dominant allele.

‘Hudson’– ‘Hudson’-NIL

HABGOOD and HAYES (1971) reported that ‘Hudson’has a single dominant gene at the Rh–Rh3–Rh4 locuson chromosome 3H. GRANER and TEKAUZ (1996)have mapped the Rh1 gene on chromosome 3H andthe same is also present in ‘Brier’. However,BJO�RNSTAD et al. (2002) have designated this locus asRrs1Brier. This is not same gene as in ‘Brier’-NIL.

‘Hudson’ was ‘R’, the NIL was ‘MR’ to isolate‘4004’, while with the isolate ‘2’, the donor was ‘MR’and the NIL ‘R’ type (Table 4). The transgression ofthe NIL can be attributed to the resistance allelesfrom the RP. The allele in ‘Hudson’-NIL behavedominantly when tested with the isolate ‘4004’ (Fig.1a) and recessively with isolate ‘2’ (Fig. 1b). SALA-

MATI and TRONSMO (1997) also reported that ‘Hud-son’ was susceptible to isolate ‘2’. Previous testsshowed that ‘Hudson’-NIL had weaker resistancethan the donor, exhibiting delayed symptom develop-ment leading even to ‘MS’– ‘S’ phenotypes with ne-crotic spots (BJO�RNSTAD, unpubl.).

V. Patil et al.196 Hereditas 137 (2002)

‘Abyssinian’– ‘Abyssinian’-NIL

Resistance in ‘Abyssinian’ is reported to be controlledby a single gene with incomplete dominance anddesignated as Rh9 (BAKER and LARTER 1963). Onthe contrary, GRO�NNERO�D et al. (2002) did not findthe Rh9 gene in ‘Abyssinian’-NIL, but instead a locuson the centromeric region of chromosome 3H. Theseresults were further confirmed by BJO�RNSTAD et al.(2002) and they have designated the alleleRrs1Abyssinian.

The recessiveness of the ‘Abyssinian’ allele ob-served by GRO�NNERO�D et al. (2002) was in agree-ment with ‘Abyssinian’-NIL when tested with isolate‘4004’ (Fig. 1a). However, the allele behaved domi-nantly with isolate ‘2’ (Fig. 1b).

Conclusions

The phenotypic resistance of barley to R. secalis is acomplex result of plant genotype, isolate, environ-mental conditions and possibly inoculum dosage ef-fects. However, they may be deciphered by carefulanalyses. Our diallel study confirmed the markeranalysis of BJO�RNSTAD et al. (2002), that among the9 NILs, 7 have scald resistance genes at the Rrs1locus, in ‘Atlas 46’-NIL at Rrs2, while in the case of‘Hudson’-NIL it was not located. The gene action isin several cases strongly dependent on the isolateused, but in other cases consistent. The resistancealleles in the RP and donors to isolate ‘2’ act addi-tively in the NILs. The 9 NILs along with two otherswere also tested with 7 differential isolates in Norwayand Canada and the results were quite consistent(BJO�RNSTAD et al. 2002). The present group of NILsinclude most of the major resistance genes to barleyscald, the exceptions being the genes identified in H.spontaneum lines.

Heterogeneity in landraces or other donors as wellas synonyms may lead to confusion when used asdifferentials (PATIL 2001). Therefore the presentNILs may give a better insight in understanding thehost–parasite interactions, in this complex systemand also make it easier to breed for scald resistance inthe future.

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