| dc.description.abstract | Gray leaf spot (GLS) caused by Cercospora zea-maydis is recognized as one of the most
yield limiting diseases of maize world-wide. In susceptible genotypes, yieldlosses of up to 60
percent are not uncommon. The objectives of the study were to evaluate the response of
diverse maize genotypes to Gray leaf spot (GLS) infestation in western Kenya, and to
determine the genetics ofGLS resistance in two maize inbred lines (CML312 and CML389).
Another was to evaluate the relationship between GLS assessment methods, severity and
lesion length. A total of 16 hybrids were evaluated for yield and yield components under
artificial GLS infestation during the 2007/08 seasons at Maseno and at Bungoma .. Other
genotypes evaluated included, 13 inbred lines, 2 FI hybrids, and F2 populations of crosses
MSN21 and CML389 or CML312. Among the inbred lines, MSN21 was the most susceptible
to GLS and had the highest disease severity rating. The inbred linesCML389 and CML388
and their FJ hybrids showed high levels ofGLS resistance. CML312 and CML384 showed
tolerance to GLS. There was a very good correlation between the lesion length and severity
ratings (r=0.9), suggesting that both could be used in disease damage assessment.
The best hybrid for GLS resistance was the experimental EH9; however, it had lower grain
yields compared to others. The commercial hybrids PhB3253 and Kenya Seed H516 were
the most susceptible to GLS. Fifty percent of the experimental hybrids performed better than
the commercial check hybrids for grain yield under artificial GLS infestation. The best hybrid
was the experimental EHI0, with 32% yield advantage over the commercial checks. The
frequency distribution of severity data for the F2 population of a cross between MSN21 and
CML312 was continuous, suggesting that GLS tolerance is influenced by quantitative genes.
A similar frequency distribution data for F2 population of a cross between MSN21 and
CML389, showed 2 distinct peaks, and the genotypes Within the 2 classes fitted a 9 to 7 ratio.
This suggests that the resistance to GLS in CML389 may be conditioned by at least 2 major
genes, with complementary epistatic interactions. | en_US |
