DREB-D1 .

Note: BW = CIMMYT wheat accession number. BDV2

7Ai#1L group.7DL = T7DS.7DL7Ai#1L 0182, 552.

7DL-7EL 10157.

sb2 . [ Tsn1 11255.

QTL Yangmai 6 (R)/Sonalika (S): RIL population: AUDPC was controlled by four QTLs derived from Yangmai 6, viz. QSb.bhu-2AL ( Xbarc353-2A – Xgwm445-2A , R[2] =0.148), QSb.bhu-2BS ( Xgwm148-2B – Xgwm375-2B , R[2] =0.205), QSb.bhu-5BL ( Xgwm67-5BL – Xgwm371-5BL , R[2] =0.386) and QSb.bhu-6DL ( Xbarc173-6D – Xgwm732-6DL , R[2] =0.225) 10719.

939; Festival 1554; Fram I 130; Huron CI 3315 1175,1554; Kenora 1554; Kenya W744 = C6041 1175,130; Norka 1175,130; Pika 130; Sweden W1230 1554; Thew 1175; TU 4 130; Zhengzhou 871124 570.

**PM2** TraesCS5D01G044600 11503.

[ Mlx {10885D 1007; Pm48 10935. 5DS945.

Several alleles of Pm2 with wheat and alien origins have been reported in Chinese genotypes – see temporary designations. The complex nature of temporarily named powdery mildew resistance genes in the Pm2 region is discussed in 11380. Several alleged alleles at the Pm2 locus are likely Pm2a 11503.

1AS 947, 943.

The Pm3a, Pm3b, Pm3d and Pm3f alleles form a true allelic series based on sequence analysis 10292. Following the cloning and sequencing of Pm3b 10064, 6 other alleles were sequenced 10405. The Chinese Spring (susceptible) allele, Pm3CS , considered to be ancestral and present in many hexaploid and tetraploid wheats, was also transcribed {10405, 10406}. Other wheats possessed a truncated sequence (e.g. Kavkaz), or were null 10405,10406. Unique markers were developed for all 8 transcribed alleles, and for individual alleles 10405. Alleles Pm3b, Pm3d , and Pm3f were detected in Scandinavian varieties using allele-specific markers 10681.

TraesSYM2A03G00828360 11774.

2° 52. 2AL 1464.

A recessive resistance gene ( pmXXM 11661) in Xiaomaomai had a similar protein structure to Pm4d , Pm4e and Pm4h 11661. Pm4f . v: WATDE0571 11775. Pm4g . v: WW-740 11775. Pm4h . v: WW-474 11774. Pm4i . v: WATDE0048 11775. Pm4j . v: WATDE0592 11775. Add note at end of Pm4 section: Some variants of PM4 confer resistance to wheat blast {11632, 11735, 11775} – see Reaction to Magnaporthe grisea .

TraesCS7B02G441700 (susceptible allele) (chr7B: 706.811-706.816 Mb) 11533.

Although Duanganmang ( PmDGM ) had an identical sequence and UTR to Pm5e , a second completely linked gene was postulated to account for a different response pattern to the Pm5e control 11705. pm5.

C 626; Abe 97,1256; Coker747 {786, 1079}; Mengavi 97; Oasis 786; Timgalen 98; TP 114/2[*] Starke deriv. B 626.

4BL-5RL 543, but more recently revised to T4BS.4BL-2R#IL 389, 380.

1R(1B).

6SL 572, 598. 6S[1] S 598.

3BS-3S[1] #1S.

Pm14 and Pm15 were detected using hybrids between B. g. tritici and B. g. agropyri cultures.

Pm14 and Pm15 were detected using hybrids between B. g. tritici and B. g. agropyri cultures.

To account for the different chromosome locations a 4A-4B translocation was suggested 10217. Based on the 5B location and similar disease responses Pm16 and Pm30 may be the same 10217.

Deleted, see Pm1c .

6BL = T6BS.6R#2L 386, 389, 543.

6VS#2 {1177, 11714}.

Deleted. Pm22 . Deleted, renamed as Pm1e

Deleted. Pm23 . Deleted, Renamed as Pm4c . PM24 . TraesCS1D02G058900; AET1Gv20142700. This locus is also named RMG1 ( RWT4 ) – see Reaction to Magniporthe grisea .

Linked with 3 RAPDs, the nearest, OPAG04950, at 12.8 +/- 4.0 cM 1343; Associated with 3 RAPDs 1344.

PM31 Deleted. This gene designation 0301 is not valid; subsequent studies 10918 showed the gene is Pm21 .

A further gene derived from T. monococcum PI 427772 was identified in BCBGT96A = PI 599036 = Saluda*3/PI 427772 10479. A single resistance gene was identified on chromosome 7AL in hexaploid germplasm NC96BGT4 (a T. monococcum derivative). This gene was proximal to Pm1 and considered to be different from Pm37 , although possibly allelic 10274. **PM38** TraesCS7D03G0183600

triticina , Reaction to P. striiformis .

**bin:

PM53 Curator’s note: A publication of this gene could not be located.

5AS (5VS.5AL) 11108. 5DS (5VS.5DL) 11109.

5VS) 11109.

6RS) 11155.

Putative Pm65 allele 11752. Pm351817 11752.

1VS#5) 11426.

Pm8 was suppressed when locus Pm3 is transcribed (including Chinese Spring and Thatcher which have no currently detectable Pm3 resistance alleles) 10828.

PMTR1 & **PMTR3I.** SECCE6Rv1G0382290 . PmTR1 &

6VS#4S 11703.

Pm6S[l] conferred resistance to 28 of 30 Chinese Bgt isolates 11597.

Recessive 10604. 5A[m] L 10604.

Three of 61 Israeli Bgt isolates were avirulent: all three isolates were from tetraploid wheat accessions. It is possible that the gene may be present in many common wheat accessions.

v: LS5082 11629. ma: Located in the interval 710.3 – 711.0 Mb 11629.

TA2682c carries a second dominant gene located in chromosome 1A 10175.

Unnnamed resistance gene 11612. WTK4 11612. 7D 11612.

Xbarc148-1A – Xgwmc550-1A interval. R[2] =0.074-0.099; QPm.caas-4DL proximal to Xwmc331-4D . R[2] =0.15-0.23; QPm.caas-6BS , proximal to Xbarc79-6BS , R[2] =0.09-0.13; and QPm.caas-7AL , proximal to Xbarc174-7AL , R[2] =0.067-0.071 10680. Additional temporarily named genes and QTL are listed in 11655.

Susceptibility to this non-pathogen of common wheat is rare, with only one susceptible genotype being documented. A few susceptible tetraploid genotypes were identified 10939.

VIGS silencing of 5AL-B4 on chromosome 5A compromised resistance conferred by Dn1 suggesting a decoy role 11333. Tests of allelism indicated that Dn1, Dn2, Dn5, Dn6, and Dnx and four uncharacterized lines were identical or closely linked 11225.

According to Saidi & Quick 1250, Dn1 and Dn2 are probably allelic. Reference stocks with each gene showed allelism with a gene in PI 262605.

Dn4 and an uncharacterized gene in PI 151918 were allelic or tightly linked 11225.

7DL 287, 10396, 10310.

1B = 1BL.1RS 9918.

QTL QTLs for antixenosis were associated with Xpsr687-7D (7DS) and Xgwm437-7D (7DL) in CS/CS (Synthetic 7D) 10136. Separate antibiotic effects were demonstrated for the same chromosome 10136. A QTL, QDn.unlp.6A , for antixenosis was associated with Xgwm1393-6AL and Xgwm1150-6AL in a CS/CS(Synthetic 6A) DH population 10216.

The relationship of Fhb1 to Fhs1 or Fhsb2 1096 is unknown. Lines combining Fhb1 and Sr2 are reported in 11170; Fhb1 is located about 2 cM proximal to Sr2 . SYN1 / Ocoroni DH population: three QTL from SYN1 were identified, QFhs.cim-2D (PVE 25%), QFhs.cim-7A (PVE 4.7%) and Qfhs.cim-7A (PVE 4.2%) 11165. A marker study found that 14 of 66 wheats with putative FHB resistance shared markers indicative of the 3BS QTL in Ning 7840, Sumai 3, Wangshuibai and possibly Wuhan 3, plus Japanese landraces Shinchunaga and Shirasu No 1 10115. The original source may be the landrace 'Taiwan Wheat' rather than Funo 10115.

7Lr#1S10529.

Although plants with Fhb-4 were taller than the recurrent parent, the height difference was not associated with the Rht-B1 locus 10885. Type I resistance (% infected plants) in this cross was attributed to 10 chromosome regions among which Qfhi.nau-4B ( Xwmc349-4B – Xgwm149-4B - r[2 ] = 0.75), XFhi.nau-5A (Xwmc96-5A – Xgwm304-5A - R[2 ] = 0.27) and Qfhi.nau-5B (Xgwm408-5B – Xbarc140-5B ) from Wangshuibai were detected in at least 3 of 4 years 10282. A significant additive effect of QTL on 6D and 2A was also observed 10282.

Closely linked in coupling with Qflw.nau-5A for narrow leaf width, but recombination is reported in 11041. According to 11487 Fhb5 might be the same as Qfhs.ifa-5Ac but the issue remained ambivalent.

T1AL.1AS-1E[ts] #1S 11048

T7DS.7D1-7e12L 11060

QTL QTLs for resistance to Fusarium graminearum detected in the cross Renan/Recital 10069. All resistance alleles, except QFhs.inra-3A , were contributed by Renan. LOD scores and percent of variation explained by the QT (R[2] ) are average of three years of field tests.

This QTL explained 42% of the variation in Sumai 3/Stoa 0175. Two additional QTL for resistance to Fusarium graminearum were identified in the croSumai3/Stoa 0175. The QTL on 4BS was associated with Xwg909-4B and the QTL on 6BS was associated with Xbarc101-6B and Xbcd1383-6B 0175. The QTL associated with markers Xgwm493-3B/Xgwm533-3B (explaining 24.8 % of the variation), and Xbarc101-6B/Xbcd1383-6B were also identified in a RIL population from the cross ND2603/Butte 86 0175. In addition, one QTL on chromosome 3AL associated with Xbcd941-3A and one on chromosome 6AS associated with XksuH4-6A were identified in RILs from the cross ND2603/Butte 86 0175. Remus / CM-82036 (a Sumai 3 derivative): DH population: Resistance QTL on chromosome 3BS associated with Xgwm493-3B and Xgwm533-3B 0240. Additional QTL in this cross were detected on chromosome 5A, associated with Xgwm293-5A and Xgwm304-5A , and possibly on 1B, associated with Glu-B1 0240. Two major genes with additive effects were reported in crosses between Sumai 3 (resistant) and two susceptible cultivars 0174. One of the genes was assigned to 5AL based on linkage to the dominant awn suppressor B1 (RF 15.1-21.4%). Alve (S) / Line 685 R: DH population: QTL on chromosomes 4D ( Rht-D1 ), 3BS, 5A and 2BL 10972. Two resistance QTL were needed to counteract the negative effect of the Rht-D1b semi-dwarfing allele 10972. Arina (R) / Forno (S): Three QTLs, QFhs.fal-6DL (R[2] =22%), QFhs.fal-5BL.1 (in Forno, R[2] =14%) and QFhs.fal.4AL (R[2] =10%) and 5 minor QTLs in 2AL, 3AL, 3BL, 3DS and 5DL were detected 10172. Arina / Riband DH lines: QTL affecting ADUPC were identified in 1BL(2), 2B, 4DS, 6BL and 7AL (Arina), and 7AL and 7BL (Riband). The most effective was the 4DS QTL that appeared to be an effect of Rht-D1a rather than height per se 10464. Baishanyuehuang (R) / Jagger (S): RIL population: Four genes/QTLs derived from the resistant parent included Fhd1 (R[2] =0.16), Qfhb.hwwg-3BS c (R[2] =0.09), Qfhb.hwwg-3A (R[2] =0.05-0.08) and Qfhd.hwwg-5A (R[2] =0.05 in one trial) 10950. Cansas (moderately resistant) / Ritmo (susceptible): Map based analysis across environments revealed seven QTL, QFhs.whs-1BS (1RS), QFhs.whs-3B (not Fhb1 ), QFhs.whs-3DL, QFhs.whs-5BL '(renamed Qfhs.lfl-1BL in 10768)' , QFhs.whs-7AL and QFhs.whs-7BL (cumultatively, R[2] = 0.56). The chromosome 1D gene was primarily involved in resistance to fungal penetration and the others in resistance to spread 10503. There were significant correlations of FHB response with height and heading date 10503. Qfhs.lfl-1BL was verified in F4:7 lines and detected in Biscay, History and Pirat 10768. The renamed Qfhs.lfl-1BL reduced FHB severity by 42% relative to lines lacking it 10698. This gene was also present in Biscay, History and Pirat 10698. CS / CS(Sumai 3 7A): QFhb7AC , nearest marker Xwmc17-7A , explained 22% of phenotypic variance for Type II and 24% of phenotypic variance for Type III resistance 10798. Chris / Frontana: In a reciprocal backcross analysis of Chris monosomics/Frontana, Frontana chromosomes 3A, 6A and 4D reduced visibly diseased kernels, kernel weight and DON content, whereas Frontana chromosomes 2A, 2B, 4B and 7A increased the same traits 10398. Further study of the 3A, 6A and 4D reciprocal substitution lines indicated that chromosome 3A of Frontana had the largest effect on incidence, severity, spread and kernel damage, 4D less so and 6A possibly not at all 10900. DH181(R)(Sumai 3 / HY 386 Seln.): QTL identified in 2DS, 3AS, 3BS, 3B Cent. region, 4DL, 5AS, 6BS 10213. Dream(R) / Lynx(S): RIL population: Following inoculation with F. culmorum 4 QTL for AUDPC were identified on chromosomes 6AL (R[2] =19%), 1B (12%), 2BL (11%) and 7BS (21%). The resistance allele in 1B came from Lynx and was associated with T1BL.1RS 10260. Dream*4 / Lynx lines were developed by selection of QTL on chromosomes 6AL, 7BS and 2BL. Lines carrying QFhs.lfl-6AL and QFhs.lfl-7BS were more resistant than lines lacking them; the 2BL QTL effect was not verified 10470. Chokwang (R) / Clark (S): Qfhb.ksu-5DL.1 associated with Xbarc239-5D (R[2] =0.24) 10276, Qfhb.ksu4BL.1 associated with Xbarc1096-4B (R[2] =0.13) 10276, and Qfhs.ksu-3BS.1 marginally associated with the region of Fhb1 (R[2] =0.1) 10276.Ernie (Res) / MO94-317 (Sus): 243 F8 RIL population. Four QTLs from Ernie detected as follows: Qfhs.umc-2B , linked to Xgwm278-2BS , R[2] = 0.04 10456; Qfhs.umc-3B , linked to Xgwm285-3BS , R[2] = 0.13 10456; Qfhs.umc-4B , linked to Xgwm495-4BL , R[2] = 0.09 10456. Qfhs.umc-5A , linked to Xgwm165-5A , R[2] = 0.17 10456. Evidence was provided to suggest the QTL acted additively 10456. Frontana (R) / Remus (S): Major QTLs in chromosomes 3AL ( Xgwm270-3AL – Xdupw227-3A region) and 5A ( Xgwm129-5A – Xbarc-5A region) accounted for 16% and 9% of the phenotypic variation (mainly type 1 resistance) over 3 years 10174. Frontana (MR) / Seri82 (S): F3 and F3:5 populations: QTLs were located in chromosomes 1BL (R[2] =7.9%), flanked by AFLP markers, 3AL (R[2] =7.7%), flanked by Xgwm720-3A and Xgwm121-3A , and 7AS (R[2] =7.6%), flanked by anAFLP and Xgwm233-7A 10349. G16-92 (R) / Hussar (S): Two QTL for resistance to F. culmorum were identified on chromosome 1A (resistance from Hussar) (R[2] = 0.01) and 2B (resistance from G16-92) (R[2] = 0.14) 10588. Glenn (R) / MN00261-4 (S): RIL population: three of 15 QTL for FHB response and heading date were stable and explained >10% of the phenotypic variation; these were located on chromosome arms 5BL, 6BS (possibly Fhb2 ) and 7AS 11568. Grandin (S) / PI277012 (I): DH population: Two QTLs, Qfhb.rwg-5A.1 on 5AS (R[2] 0.06-0.2) and Qfhb.rwg-5A.2 on 5AL (R[2] =0.12-0.2) conferred type I and II resistance and reduced DON content 0147. The new QTL on 5AL was closely but not completely linked with gene q which is present in PI277012 10860. Hobbit Sib / T. macha

7DL-7el2 10489. 7el210489.

segregation with Xcsl107-2B . Four of 6 land varieties possessed Xcsl107-2B . A variant haplotype of Xcsl107-2B was present in AUS4930 10013; Xcdo36-2B – 7.5 cM – Xbcd1231-2B/XAtPPr5/Xcsl1072B/Cre1 10013.

2AS 0107 = 2A-2N[v] -6N[v] .

6BL 0220, on basis of linkage with Xbcd1-6B and Xcdo347-6B 220.

Qcre.src-1B was located to the Xwmc719-1B (R[2] =12%) – Xgwm140-1B (R[2] =12%) region in Trident/Molineux 10343. For review 11309.

RMG6 . TraesCS1D02G029900 .

Rmg6 was present in 77% of surveyed genotypes 11470}. Xwmc432-1D – RMG9 – 5.0 cM – RMG6 – Xwmc222-1D 11504. A second gene in chromosome 1D designated Rwt4 0302 ( TraesCS1D02G058900 11632) (was present in CS and Norin 4.

Among PM4 alleles Pm4a, Pm4b and Pm4d conferred resistance to both MoT and Bgt ; Pm5f conferred resistance to MoT but not Bgt , and Pm4f was ineffective against both pathogens 11735.

RmgGR119 confers resistance to the wheat form of the pathogen and its response is enhanced in combination with Rmg8 11263. Near-isogenic lines with the T2A-2NS translocation from Ae. ventricosa displayed reduced levels of spike blast, but there was little effect on seedling leaf blast response 11265:

v2 Chinese Spring Rmg6 11504.

RmgTd(t) was detected with a white culture of an Avena pathogen isolate backcrossed to a wheat isolate. A virulence to RmgTd(t) was completely associated with white color of the pathgen isolate 10949. The white color appeared as a mutant variant during backcrossing. The wheat blast pathogen became established on wheat cultivar Anahuac ( rmg1 rmg6 ) in Brazil in the mid-1980s. It was initially avirulent on cultivars such as IAC-5 with Rmg6 but later acquired virulence allowing it to attack most wheat genotypes 11470.

Allan et al. 019 considered that H3 and H4 might be allelic. Also suggested by Shands and Cartwright 1317. Linkage of 10.5 +/- 2% involving H3 and Pm3a in PI 468960 was attributed to a chromosome 1A/5A translocation 1437.

Recessive. 1AS 11634. H4 confered resistance to race A, but not to race B.

H7. 6AS 11511; 5D 026.

Based on the location of H9 on chromosome 1AS, H15 may also be located on chromosome 1AS 10231.

2R#2L 389.

6BL-6R#1L 389

H26 is very close to H32 10846. H27

Halotype analysis was used to postulate Ae. tauschii -derived genes H13, H22, H23, H26 and H32 in a set of synthetic wheat lines 10983. H35 in chromosome arm 3BS and H36 in chromosome arm 7AS were named for one major and one minor QTL in common wheat line SD06165 11512. Temporary designations:

A recombination value of 12.0% between leaf-rust reaction {possibly Lr10 } and Hessian-fly reaction in Selection 5240 was reported 018.

Duster (R) / Billings: DH population: QHf.osu.1A.2 (Syn. QHf.osu-1A[d] ), R[2] = 0.88, delimited to a 2.7 cM region flanked by GBS07851 and GBS10205 11324. This was a distinct locus 11.2 cM proximal to QHf.osu.1A . Jagger (S) / 2174 9 (R): RIL population: QHf.osu-1A (Syn. Qhf.osu[74] (R[2] = 0.70) and QHf.osu-2A (R[2] = 0.18) 11325. The QTL in chromosome 1A appeared to be co-linear with several previously named H genes in tetraploid wheat; the gene in 2A was in repulsion with the 2N segment present in Jagger 11325.

10486; May be the same as CreY (see reaction to Heterodera avenae ) on chromosome 3S[V] from Ae. variabilis translocated to 3BL 10800.

6D, 10105 (according to 10556 this location is not correct.

0187; Israel 493 11446; Longbow 11446; Olaf 11446; Sears' Synthetic 0186; Senat 11446; Shafir 0; Veranopolis 11446; Vivant 0187.