Inheritance and Gene Effect of Resistance to Mungbean Yellow Mosaic Virus (MYMV) in Mungbean [Vigna radiata (L.) Wilczek]

The study was conducted at Food Legumes Section, Department of Agricultural Research (DAR), Yezin, Myanmar (19°51' N latitude and 96°7' E longitude at 97 m altitude) in summer (February-May, a hot spot season for MYMV disease), 2019. The materials of this study were consisted of five mungbean genotypes, viz. two resistant genotypes (7639 and 10266) and three susceptible genotypes (7621, 10257 and R-021018) to develop F₁, F2, BC₁ (F₁P₁) and BC₂ (F₁P₂). Origin, disease reaction and some good characters of parental genotypes were presented in Table 1. These resistant genotypes and susceptible varieties were crossed by the procedure of Khattak et al., (1998) and each cross combination (F₁) raised as F₂, BC₁ (F₁P₁) and BC₂ (F₁P₂). The six basic populations, namely P_l, P₂, F_l, BC₁, BC₂ and F₂ of each combination will be grown in compact family block design with three replications. Each plot consisted of 3-m rows with inter and intra row spacing of 30 and 10 cm, respectively. The parents (P₁, P₂), F₁, BC₁ (F₁ × P₁) and BC₂ (F₁ × P₂) were sown in single row with 3m long (30 plants) and 5 row (150 plants) in F₂ for one family. All recommended cultural practices were followed, except insecticide is not spraying to allow the growth and development of vector Bemecia tabaci. Disease reaction of mungbean yellow mosaic virus was recorded at 60 days after sowing (when 95% of the spreader rows (Yezin-9) showed MYMV incidence) under field conditions. The tested populations were classified into six reactions that is, highly susceptible (HS), susceptible (S), moderately susceptible (MS), moderately resistant (MR), resistant (R) and highly resistant (HR) on the basis of disease scores and type of symptoms by estimating the average score for the top 5 leaves of each plant within each lines at 60 days after planting by Nair et al., (2017). The plants in the F₂ and back cross generations will be classified as resistant (1-3) and susceptible (4-6) following Reddy and Singh (1993).
 

 
Statistical Analysis
 
The chi-square test was performed to determine the goodness of fit of observed segregation for MYMV disease reaction in F₂ and test cross generations for the inheritance pattern of MYMV. The generation mean analysis was performed for the estimation of genetic components by scaling test for A, B, C and D scales as suggested by Mather and Jinks (1971) and Hayman and Mather (1955) and joint scaling test by Cavalli (1952) and estimation of gene effects by the model of the model of Jinks and Jones (1958). The minimum number of gene or number of effective factors controlling resistance was estimated by three methods: Method 1 was proposed by Wright (1968); Methods 2 and 3 were proposed by Lande (1981).

The number of plants, disease reaction and chi square value of parent 1, parent 2, F₁, F₂, BC₁ and BC₂ of six crosses were presented in Table 2. According to the results, the F₁ of all six crosses obviously showed that susceptibility to MYMV was dominant over resistance and no maternal effect on the inheritance pattern of MYMV in mungbean. This finding was very close agreement with the research of Khattak et al., (2000) and Shukla et al., (1978) in mungbean. Moreover, the segregation ratio of F₂ and BC₂ was observed with 1R:3S and 1R:1S, respectively and all these crosses verified that it is a single recessive gene inherited character with dominance effect of susceptibility over resistance to MYMV.  The pattern of monogenic recessive inheritance for MYMV has been reported by Sandhiya and Saravanan (2020); Basavaraja et al., (2017); Sai et al., (2017); Jain et al., (2013); Reddy, (2009). There are, however, many research findings that documented with monogenic dominant gene (Gupta et al. (2005); Sandhu et al., (1985), two recessive genes (Alam et al., (2014); Singh et al., (2013); Dhole and Reddy (2012), complementary recessive genes (Thamodhran et al., (1988) and Shukla and Pandya (1985) and two dominant genes (Mahalingam et al., (2018) and Murugan and Nadarajan (2012).
 

 
The result of scaling and joint scaling test by Mather (1949) and Cavalli (1952) for the present or absence of gene interaction was shown in Table 3. The research revealed that the scaling test A, B, C and D were not significant from zero in all crosses except from 10257 × 7639 and R-021018 × 7639. This indicated that the presence of additive × dominance interaction in 10257 × 7639 and dominance × dominance interaction in 21018 × 7639, respectively. However, when the results were subjected to confirm for the scaling test by joint scaling test, all the crosses were found with non-significant values of chi square test. The range of chi square values from the estimate of MYMV was 0.74 and 6.74, respectively. All the values were less than the 0.05 at df = 3 (7.81). Therefore, this is clearly indicated that resistance of MYMV was controlled by allelic gene action with no epistatic gene interaction and revealed the adequacy of the simple additive-dominance model which is appropriate to describe the inheritance of MYMV in the respective cross.
 

 
Genetic effects viz, m, d and h for resistance of MYMV in six mungbean crosses were presented in Table 4 according to the three parameter model by Jinks and Jones (1958). The mid parent value was significant in all crosses and expressed with the value of 3.58, 3.78, 4.19, 3.96, 3.77 and 3.45 in the cross of 7621 × 7639, 10257 × 7639, R-021018 × 7639, 7621 × 10266, 10257 × 10266 and R-021018 × 10266, respectively. This finding pointed that this MYMV resistance was quantitatively inherited. The three parameter model pronounced that only additive gene effect was found in all crosses and more pronounced significant with the value of 2.42, 2.40, 2.48, 2.44, 2.47 and 2.48 in the cross of 7621 × 7639, 10257 × 7639, R-021018 × 7639, 7621 × 10266, 10257 × 10266 and R-021018 × 10266, respectively while the no significant dominance gene effects were observed in all crosses. The plus sign in the additive gene effect implies that P1 contributes positively to the trait as compared to P2 and vice versa. This finding was more closely related with the results of gene effects for powdery mildew in mungbean and late leaf spot in groundnut by Wambi et al., (2014) and Sorajjapinun et al., (2005) who observed that additive gene action was a major role in controlling powdery mildew resistance in mungbean and late leaf spot in groundnut. The estimates of effective factor or minimum number of gene for resistance of MYMV in six mungbean crosses ranged from 0.43-1.09, 0.49-1.05, 0.54 -1.38, 0.46-1.18, 0.52-1.20 and 0.53-1.27 in the cross of  7621 × 7639, 10257 × 7639, R-021018 × 7639, 7621 × 10266, 10257 × 10266 and R-021018 × 10266, respectively (Table 5). The average number of effective factor was found with below one in all crosses of this study. Therefore, the resistance of MYMV was governed by only one gene. However, MYMV resistance in mungbean was controlled by at least two genes according to the findings of Alam et al., (2014) and Singh et al., (2013), respectively.
 

 

Based on the result of this study, it can be concluded that additive gene action was the major role for the selection of MYMV resistance. Susceptible behavior indicated as dominant over resistant and single recessive gene that controlled for the resistance of MYMV. Therefore, the knowledge of mode of inheritance and gene effects of MYMV resistance is very useful and effectively for the development of genotypes resistant to disease or incorporation of resistance into the desirable promising genotypes which have lack of disease resistance. The expression of gene contributing for MYMV resistance from others findings might be attributed due to the sources of resistant genotypes which have different nature of resistant gene used in this investigation.