In the present study for the first-time genetics and nature of gene action for resistance to bud necrosis disease in tomato was deciphered based on mechanical sap inoculation under the environment-controlled glasshouse conditions with the pure culture of GBNV. To accomplish this study, two resistant (IIHR-2901 and IIHR-2953) and one susceptible parent (PKM-1) were used to generate F1, F2, BC1P1 and BC1P2 populations. Castle wright estimation suggested that the trait is governed by the single gene blocks in both the crosses. Chi-square estimation also indicated that the resistance to bud necrosis disease in the cross PKM-1 × IIHR‐2901 is controlled by one or two recessive genes while in the cross PKM-1 × IIHR‐2953, it was found to be governed by one or two dominant genes based on the segregation pattern observed in F2 generation. However, the results remain inconclusive, as the segregation in backcrosses was not behaving as expected for both the crosses. This showed that the classical Mendelian genetics and additive-dominance model were inadequate to explain the genetical mechanism of resistance to bud necrosis disease of tomato. It may be either due to the presence of modifiers in the background or may be due to the presence of epistatic interactions. Later, in this study presence of epistatic interaction was confirmed by the significance of scaling test in both the crosses. Estimates of six parameters [m, d, h, i, j and l] through generation mean analysis, suggested the preponderance of non-allelic interactions mostly of additive × dominance [j] type with negative signs in both the crosses and additive × additive [i] interaction with positive sign in the cross between PKM-1 × IIHR‐2953. Complementary type of epistasis has been observed for both the crosses as both the components viz., dominance [h] and dominance × dominance [l] were in similar direction. Hence, all the above results indicated that the improvement for resistance to bud necrosis disease could be possible through recombination breeding, hybridization followed by selection at later generations with more emphasis on selection between families and lines.

中文翻译：

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花生芽坏死病毒（GBNV）引起番茄（Solanum lycopersicum L.）芽坏死病的遗传分析

在本研究中，首次对番茄芽坏死病抗性基因作用的遗传学和性质进行了破译，该研究基于 GBNV 纯培养物在环境控制温室条件下的机械接种。为了完成这项研究，使用两个抗性（IIHR-2901 和 IIHR-2953）和一个易感亲本（PKM-1）来生成 F1、F2、BC1P1 和 BC1P2 种群。Castle Wright 估计表明，该性状受两个杂交中的单个基因块控制。卡方估计还表明，PKM-1 × IIHR-2901 对芽坏死病的抗性受一个或两个隐性基因控制，而在 PKM-1 × IIHR-2953 杂交中，发现它受基于在 F2 代中观察到的分离模式的一个或两个显性基因。然而，结果仍然没有定论，因为回交中的分离并没有像两个杂交预期的那样表现。这表明经典的孟德尔遗传学和加性优势模型不足以解释番茄芽坏死病抗性的遗传机制。这可能是由于背景中存在修饰符，也可能是由于存在上位相互作用。后来，在这项研究中，两个十字架中缩放测试的重要性证实了上位相互作用的存在。通过生成均值分析估计六个参数 [m, d, h, i, j 和 l]，表明非等位基因相互作用的优势主要是加性 × 优势 [j] 类型，在交叉中带有负号，而加性 × 加性 [i] 相互作用在 PKM-1 × IIHR-2953 之间的交叉中带有正号。已经观察到两个交叉的互补类型的上位性，因为这两个组成部分，即优势 [h] 和优势 × 优势 [l] 的方向相似。因此，上述所有结果表明，通过重组育种、杂交和后代选择，更强调家系和品系之间的选择，可以提高对芽坏死病的抗性。