(Loegering and Sears, 1966) (Plate 3-4)


Sr7 (Knott and Anderson, 1956).

Low Infection Type

1 to 3C (Knott, 1989); yellow chlorosis/necrosis surrounding uredia is common and characteristic.

Environmental Variability

Presumed to be low.


Common wheat. Sr7a was originally identified in a number of Kenyan wheats (Knott and Anderson, 1956; Knott, 1962a).

Pathogenic Variability

Virulence occurs in most geographic areas (Luig, 1983; Huerta-Espino, 1992). Intermediate low responses are common. In addition, host genetic background probably has a significant influence on response (Roelfs and McVey, 1979).

Reference Stocks

i: Egypt Na 101/6*Marquis; Kenya 117A/6*Marquis (Green et al., 1960); Sr7a/9*LMPG (Knott, 1990); Sr7a/10*Marquis (Knott, 1965).

s: Chinese Spring*7/Kenya Farmer 4A; Chinese Spring*8/Sapporo 4A (Loegering and Sears, 1966).

v: Kenya 117A C.I. 13140 Sr9b (Knott, 1957b). Egypt Na 101 P.I. 139599 Sr9b Sr10 (Knott, 1957a).

Source Stocks

See lists in Luig (1983) and McIntosh (1988a).

Africa: Kentana 52 Sr6. Kenya wheats (Knott, 1957a, 1957b, 1959, 1962a).

Australia: Khapstein Sr2 Sr13 Sr14 (Knott 1962b). Mendos Sr11 Sr17 Sr36. Chris derivative W3747 Sr12.

Canada: Manitou Sr5 Sr6 Sr9g Sr12.

Japan: Sapporo P.I.81790-2 (Knott and Shen, 1961).

USA: Chris Sr5 Sr8a Sr9g Sr12 (Singh and McIntosh, 1987).


Seedling leaves of (L to R): Chris, Chris Derivative W3747, Mendos Derivative, Marquis + Sr7a, CS/Kenya Farmer 4A, Sr7a/9*tMPG, Chinese Spring and Marquis; infected with A. pt. 116-2, 3, 7 and B. yellow culture 80-E-2. The first six wheats carry Sr7a. However, Chris and Chris Derivative show lower responses to both cultures due to avirulence for Sr5 in the former, and avirulence for additional genes in the latter. Note the lower pathogenicity of culture 80-E-2 on seedlings with Sr7a and the lower pathogenicity of pt. 116-2, 3, 7 on Marquis relative to Chinese Spring.


Use in Agriculture

Sr7a has not been added purposefully as a means of achieving resistance, and has been found in wheats studied after commercial release. Singh and McIntosh (1986b) reported interactions of Sr7a and Sr12 resulting in significantly higher levels of resistance than that conferred by either gene acting alone.