--S. K. Vasal, F. Gonzalez C. and G. Srinivasan
Early work at CIMMYT for resistance to the Tar Spot Complex, incited by the fungi Phyllachora maydis-Monographella maydis, indicated the presence of genetic variation for different sources of resistance to the disease. Phenotypically, some resistant plants did not have any lesions, some had small lesions, and others had normal size lesions but with slow development of the disease. Genetically, the segregation observed in families of some crosses could be explained by monogenes conferring resistance to the disease, but with different gene action (Table 1). Further analysis of generations of resistant x susceptible crosses confirmed the presence of a single dominant gene in the resistant line Pool 22 TSR-7-B-#, and a single recessive gene in the line Pool 23 TSR-40-B-# (Table 2). Two other sources of resistance which had susceptible type lesions but slow development of disease were also crossed to susceptible parents. The development of disease over time, with scores taken at three different dates (weekly intervals), are presented in Figures 1 and 2. Generation Mean Analyses (GMA) for these crosses show a relatively simple genetic control of the resistance with mainly dominant and additive effects (Table 3). These and other sources of resistance have been combined to form two yellow and two white populations which will serve as sources of resistance to Tar Spot Complex.
Table 1. Segregation for Tar Spot disease in families of the cross (PD(MS)6
H.E. 02 x Selecc. Precoz.)-B-#-#.
|No. of plants|
|Family||Res.||Susc.||Expected ratio||X2||P (%)|
|1||14||16||1 : 1||0.133||>70|
|2||14||16||1 : 1||0.133||>70|
|4||20||11||3 : 1||1.817||>10|
|9||21||9||3 : 1||0.4||>50|
|10||14||15||1 : 1||0.035||>80|
|17||24||8||3 : 1||0||>99|
|26||15||17||1 : 1||0.125||>70|
|27||15||17||1 : 1||0.125||>70|
|29||16||14||1 : 1||0.133||>70|
|30||9||21||1 : 3||0.4||>50|
|40||22||8||3 : 1||0.044||>80|
Table 2. Segregation for Tar Spot disease in two crosses involving Pool
22 TSR x Pop.26 and Pop.25 x Pool 23 TSR.
|No. of plants|
|Generation||Res.||Susc.||Expected ratio||X2||P (%)|
|Pool 22 TSR-7-B-#(P1) x Pop.26 C5 HC 37-1-4-B-#(P2)|
|P1||42||0||1 : 0||-|
|P2||0||42||0 : 1||-|
|F1||40||0||1 : 0||-|
|F2||65||17||3 : 1||0.796||>30|
|BC1||78||0||1 : 0|
|BC2||32||48||1 : 1||3.2||>5|
|Pop. 25 C0 HC 128-2-1-B-#(P1) x Pool 23 TSR-40-B-#(P2)|
|P1||35||0||1 : 0||-|
|P2||0||39||0 : 1||-|
|F1||0||42||0 : 1||-|
|F2||15||66||1 : 3||0.796||>10|
Figure 1. Progression of Tar Spot (0-10) in the cross Pool 26 TSR16-B-#(P1) x Pop. 24 C5 HC34-2-3-B-#(P2).
Figure 2. Progression of Tar Spot (0-10) in the cross Pool 19 TSR27-B-#(P1) x Pop. 23 COHCS3-31-#(P2).
Table 3. Genetic effects for resistance to Tar Spot disease in two crosses
with resistant lines from different origins.
|Mean*||Additive (A)||Dominance (D)||X2||P (%)|
|Pool 19 TSR 27-B-# x Pop.23 C0 HCS3-31-#|
|Pool 26 TSR 16-B-# x Pop.24 C5 HC34-2-3-B-#|
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