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Genetic characterization of maize doubled haploid lines for Fusarium stalk rot caused by Fusarium verticillioides
Fusarium stalk rot disease (FSR) of maize caused by Fusarium verticillioides (Sacc.) Nirenberg is becoming an important biotic production constraint in many of the major maize growing areas causing substantial yield losses. Inbreds are preferred as parents in hybrid development owing to homozygous n...
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Published in: | Journal of genetics 2020-12, Vol.99 (1), Article 83 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Fusarium stalk rot disease (FSR) of maize caused by
Fusarium verticillioides
(Sacc.) Nirenberg is becoming an important biotic production constraint in many of the major maize growing areas causing substantial yield losses. Inbreds are preferred as parents in hybrid development owing to homozygous nature and high heterotic ability. Double haploid (DH) technology has emerged as a significant milestone. A total of 339 DH lines were generated from two inbred lines, VL1043 (susceptible) and CM212 (resistant), through
in vivo
haploid induction method. The 339 DH lines along with parents were phenotyped for their response to the FSR at the College of Agriculture, V. C. Farm, Mandya, India during summer, kharif and rabi seasons of the 2019–2020. Best linear unbiased predictors (BLUPs) were estimated for the FSR disease scores over three seasons. A wide range of BLUP scores of three to nine indicated the presence of higher variation for response of DH lines to FSR disease. The higher estimates of standardized range (1.31) and phenotypic coefficient of variation (19.80) also displayed higher variability. Nine lines were moderately resistant and 188 exhibited moderately susceptible reaction. The distribution of DH lines was positively skewed (1.34) and platykurtic (2.31) which suggested complementary epistasis and involvement of large number of genes in the disease expression. |
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ISSN: | 0022-1333 0973-7731 |
DOI: | 10.1007/s12041-020-01236-4 |