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Genetics of resistance to Fusarium stalk rot caused by Fusarium verticilloides in maize (Zea mays L.)

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Fusarium stalk rot disease (FSR), incited by Fusarium verticilloides, is becoming an important biotic production constraint in many major maize growing areas causing substantial yield losses. The present investigation was conducted to understand the genetics of resistance to FSR through six generation means and variances, as a first step in addressing the problem. Five crosses were developed by crossing four FSR susceptible inbreds (VL1043, VL108867, VL121096 and VL1218) with two resistant inbreds (CM202 and CM212). Six generations of the five crosses (VL1043 × CM212, VL108867 × CM202, VL121096 × CM212, VL1218 × CM202 and VL1218 × CM212) were evaluated through artificial disease inoculation during post rainy season of 2018 and summer, 2019. The scaling tests and joint scaling tests indicated the inadequacy of additive-dominance model and showed the presence of epistatic gene effects in all the five crosses for FSR resistance. The study further revealed the importance of additive, dominance and additive × additive gene effects in the expression of FSR. The magnitude and direction of the additive genetic effects [a], dominance genetic effects [d], magnitudes of additive genetic variance (2A) and dominance genetic variance (2D) varied with the genetic background of the crosses over seasons. Duplicate gene interaction was evident in the inheritance of FSR resistance. Both, additive and non-additive components were found important thus reciprocal recurrent selection would be more effective in obtaining FSR resistant maize inbred lines.
Title: Genetics of resistance to Fusarium stalk rot caused by Fusarium verticilloides in maize (Zea mays L.)
Description:
Fusarium stalk rot disease (FSR), incited by Fusarium verticilloides, is becoming an important biotic production constraint in many major maize growing areas causing substantial yield losses.
The present investigation was conducted to understand the genetics of resistance to FSR through six generation means and variances, as a first step in addressing the problem.
Five crosses were developed by crossing four FSR susceptible inbreds (VL1043, VL108867, VL121096 and VL1218) with two resistant inbreds (CM202 and CM212).
Six generations of the five crosses (VL1043 × CM212, VL108867 × CM202, VL121096 × CM212, VL1218 × CM202 and VL1218 × CM212) were evaluated through artificial disease inoculation during post rainy season of 2018 and summer, 2019.
The scaling tests and joint scaling tests indicated the inadequacy of additive-dominance model and showed the presence of epistatic gene effects in all the five crosses for FSR resistance.
The study further revealed the importance of additive, dominance and additive × additive gene effects in the expression of FSR.
The magnitude and direction of the additive genetic effects [a], dominance genetic effects [d], magnitudes of additive genetic variance (2A) and dominance genetic variance (2D) varied with the genetic background of the crosses over seasons.
Duplicate gene interaction was evident in the inheritance of FSR resistance.
Both, additive and non-additive components were found important thus reciprocal recurrent selection would be more effective in obtaining FSR resistant maize inbred lines.

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