A maize cultivar 'Makki Safed-1' (MS1) suffered heavily due to an epiphytotic of brownstripe downy mildew during the kharif of 1975. The disease is caused by Sclerophthora rayasiae var. zeae Payak and Renfro (Phytopath. 57:394-397).
However, considerable variability was observed within the cultivar for
the reaction to this disease. This cultivar was, therefore, subjected to
mass selection before as well as after flowering. The original and improved
version, MS1 (ms)C1, were evaluated in some cross combinations at Gurdaspur
in a randomized block design with four replications. A plot consisted of
two rows, each of 6 meters length. Row-to-row distance was 75 cm and plant-to-plant
spacing was 25 cm. The experiment was planted in a sick plot created by
putting on powdered infected leaf debris. Disease incidence was recorded
on a 1-5 scale, which was adapted from Miller et al. (Pl. Dis. Reptr. 54:1134-1136,
1970). The grain yield performance and disease reaction were as follows:
|Pedigree||Reaction to BSDM*
|(CM 400 x CM 300) x MS1 (Original)||2.0||4126|
|(CM 400 x CM 300) x MS1 (ms)C1||1.5||4253|
|H 301 x MS1 (Original)||2.4||2995|
|H 301 x MS1 (ms)C1||2.2||3185|
|(Syn P200 x Kisan) x MS1 (Original)||1.6||4485|
|(Syn P200 x Kisan) x MS1 (ms)C1||1.1||4774|
|Tuxpeno Planta Baja x MS1 (Original)||1.6||4311|
|Tuxpeno Planta Baja x MS1 (ms)C1||1.1||4667|
|C.D. at 5 percent||0.8||1063|
*BSDM means brown stripe downy mildew and 1 means highly resistant and 5 highly susceptible.
The improved population was significantly better than the original population for reaction to brown stripe downy mildew. Better resistance to disease in the improved population was also evident in all the crosses. For grain yield also an appreciable gain is apparent in the crosses involving MS1 (ms)C1. The improved version has given consistently better yield performance in all the crosses.
The performance of crosses shows that the gain made in the population is at the genetic level and the superiority is transmitted to the crosses. Significant gains in the population in a cycle of mass selection indicate that inheritance of this disease may be largely under additive genetic control.
A. S. Khehra, B. S. Dhillon, V. K. Saxena, V. V. Malhotra & S. S. Pal
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