(McIntosh, 1988a) (Plate 3-37)


SrTt1 (McIntosh and Gyarfas, 1971).

Chromosome Location

2B (Nyquist, 1957); 2BS (Gyarfas, 1978). Stem rust and powdery mildew resistances in the wheats C.I. 12632 and C.I. 12633 were originally thought to be determined by duplicate linked factors (Allard and Shands, 1954) but Nyquist (1962) demonstrated that a single gene was involved with differential fertilisation resulting in variable ratios. The mildew resistance factor was subsequently designated Pm6 (Jorgensen and Jensen, 1973). In early studies at The University of Sydney, Sr36 behaved as an allele of Sr9. McIntosh and Luig (1973a) reported a rare recombinant combining Sr36 and Sr9e. The line was later designated Combination III (Luig, 1983). In further genetic studies involving this stock, Sr36 was normally transmitted and showed about 20% recombination with Sr9 (McIntosh and Luig, 1973a). Sr36 recombined with Sr9b but not with Lr23, located in chromosome 2BS. In a separate study with progeny of a monosomic 2B line derived from Combination III, chromosome misdivision products that separately carried Sr9e and Sr36 were obtained (Gyarfas, 1978). This demonstrated that the genes wete located in different chromosome arms.

Low Infection Type

Usually 0;=, but sometimes X. Apparent heterogenous infection types of 0;3 (Knott, 1990) and 0;4 (Roelfs and McVey, 1979) were reported in North America.

Environmental Variability

Under Australian greenhouse conditions, Sr36 appears to produce higher infection types in winter when both light intensity and temperatures are lower than in summer. AP Roelfs (pers. comm. 1988) observed mixed responses with some cultures in autumn and spring but not in summer or winter.


T. timopheevii. Independent transfers to hexaploid wheat resulted in C.I. 12632 and C.I. 12633 (Allard and Shands, 1954), Timvera (Pridham, 1939) and C.I.13005 (Atkins, 1967).

Pathogenic Variability

Virulence has arisen on at least two independent occasions in Australia, resulting in the susceptibility of Mengavi in 1961 (Luig and Watson, 1970) and Cook in 1984 (Zwer et al., 1992). A similar experience occurred in South Africa following the deployment of Sr36 in wheat-growing areas. In North America, early isolates of race 15B were characterised by virulence on T. timopheevii and, by inference, wheats such as C.I.12632 and C.I.12633. Later isolates of 15B were virulent on C.I.12632 and avirulent on T. timopheevii. These observations were confirmed by RA McIntosh (unpublished, 1970) working at the University of Missouri. In later studies, wheats with Sr36 were described as having low receptivity to pathotypes normally considered virulent (Rowell and McVey, 1979; Roelfs and McVey, 1979; Rowell 1981a, 1981b, 1982).

Huerta-Espino (1992) found pathogenic variation in most of the major regions from which he obtained samples. This indicated that a line with Sr36 would be a useful worldwide differential.

Reference Stocks

i: Sr36/8*LMPG (Knott, 1990); Line C, a W2691 backcross derivative with Sr36 (Luig, 1983).

v: C.I.12632 (= W1656); C.I.12633 (= W1657); Idaed 59; Mengavi; Timvera (McIntosh and Gyarfas, 1971).

Source Stocks

Australia: Songlen Sr2 Sr5 Sr6 Sr8a. Timgalen Sr5 Sr6. Cook Sr5 Sr6 Sr8a. Mendos Sr7a Sr11 Sr17. Combination III W3486 Sr9e (Luig, 1983).

Mexico: Zaragosa 75 (Le Roux and Rijkenberg, 1987b).

South Africa: Dipka; Flamink; Gouritz; SST101; SST107. See Le Roux and Rijkenberg (1987b) and Sharma and Gill (1983).

USA: Hand; Kenosha; Purdue; Roughrider; Vernum; Wisconsin Supremo. Arthur Sr2 Sr5 Sr8a; Arthur 71 Sr2 Sr5 Sr8a.


Seedling leaves of (L to R): C.I.12632 (W1656), Mengavi, Arthur, Combination III and Chinese Spring; infected with A. pt. 34-1, 2, 3, 6, 7, 8, 9 [P36] and B. pt. 34-1, 2, 3, 4, 5, 6, 7 [p36]. Arthur carries an unknown resistance to pt. 34-1, 2, 3, 4, 5, 6, 7. This resistance could be due to Sr7a whereas resistance in Combination III to this pathotype is conferred by Sr9e.


Use in Agriculture

Sr36 has been a very valuable gene for wheat production in Australia. It was initially used in cv. Mengavi which was rendered very susceptible by a new pathotype detected very soon after registration. Sr36 was then combined with Sr7a, Sr11 and Sr17 and released in cv. Mendos which in turn succumbed to stem rust after a few years. In 1967 Timgalen was released as a prime hard quality wheat in rust-prone areas. The source of Sr36 in Timgalen is unknown but is presumed to be C.I.12632 or a derivative. Timgalen was followed with the derivatives, Timson, Songlen, Shortim and Cook over subsequent years. Stem rust was found on Cook wheat in 1984 (Zwer et al., 1992). Because of the activities of the National Wheat Rust Control Program, Cook derivatives with additional resistance genes (such as Sunco with Sr24) were released in 1985 and Cook was rapidly withdrawn. The Cook-attacking pathotype then declined to negligible levels, thus providing an enhanced resistance to the Cook derivatives (Park and Wellings, 1992).

According to Roelfs and McVey (1979) and supported by the studies of Rowell (1982) some pathotypes considered virulent on lines with Sr36 developed more slowly and gave lower numbers of pustules on genotypes with Sr36. This contrasted with the Australian experience with Mengavi and Mendos which were seriously affected by the relevant virulent pathotypes.