Inheritance Pattern of Mungbean Yellow Mosaic Virus (MYMV) Disease Resistance in Blackgram [Vigna mungo (L.) Hepper]

Blackgram [Vigna mungo (L.) Hepper] is one of the important pulse crop of India. India is the largest producer and also consumer of blackgram. It is referred as the “king of the pulses” due to its delicious taste and numerous other nutritional qualities. Blackgram is superb combination of all nutrients, which contains proteins (25-26%), carbohydrates (60%), fat (1.5%), minerals, amino acids and vitamins. Among various biotic and abiotic yield limiting factors, yellow mosaic disease (YMD) caused by mungbean yellow mosaic virus (MYMV) is the most destructive limiting factor in blackgram. Infection of MYMV may cause up to 85-100% yield loss in blackgram (Singh et al., 2011). Main pathogens causing YMD in India are mungbean yellow mosaic virus (MYMV) and mungbean yellow mosaic India virus (MYMIV) (Varma and Malathi, 2003; Malathi and John, 2008).  The disease is caused by geminivirus with bipartite genomes transmitted by different species of whitefly belongs to the genus begomovirus and family geminiviridae. Infected plants are stunted in growth and usually mature late. They produce very few flowers and pods. Pods are curled and reduced in size with increased percentage of shrivelled seeds (Nariani 1960; Nene 1973). Since the virus transmission is attributed by the vector-whitefly (Bemisia tabaci), control of MYMV disease is based upon limiting the vector population by using insecticides.  However, it is ineffective under severe whitefly infestations and also not an eco-friendly approach. The most effective way to prevent the occurrence of this disease is to develop genetically resistant cultivars of blackgram. There are conflicting reports about the genetics of resistance to MYMV disease, claiming both resistance and susceptibility is controlled by dominant gene.  In blackgram, monogenic dominant nature of resistance was reported by Dahiya et al., (1977), Kaushal and Singh (1988) and Gupta et al., (2005), while it was reported to be digenic recessive by Singh (1980), Dwivedi and Singh (1985) and Verma and Singh (1986).  Monogenic recessive control of yellow mosaic resistance was also reported by some authors (Pal et al., 1991; Reddy and Singh 1995).  Hence, the present study was aimed to understand the inheritance pattern and the gene action governed by the MYMV disease resistance in eight crosses of blackgram.

The material for the present investigation consists of six parents and their eight crosses in F₂ generation. Female parents viz., MDU 1 and CO5 were highly susceptible to mungbean yellow mosaic virus (MYMV) disease.  Male parents viz., Mash 114, Mash 1008, VBN 6 and VBN 8 were resistant to MYMV disease. Eight crosses viz., MDU 1 × Mash 114, CO 5 × Mash 114, MDU 1 × Mash 1008, CO 5 × Mash 1008, MDU 1 × VBN 6, CO 5 × VBN 6, MDU 1 × VBN 8, CO 5 × VBN 8 were generated during Dec 2017- Feb 2018 under field conditions at National Pulses Research Centre, Vamban. Parents, F₁ and F₂ generation of these cross combinations were raised during July-Sep, 2018 at National Pulses Research Centre, Tamil Nadu Agricultural University, Vamban, Tamil Nadu. Each progeny was raised in one row of 3 m length with a spacing of 30 × 10 cm. Susceptible genotypes viz., CO 5 and MDU 1 were sown as disease spreader rows after every eight rows and also around the plots. All parents, F₁ and F₂ generations were screened for MYMV disease by adopting infector row method. An infector row of CO 5 was raised to intensify the MYMV disease pressure after every eight rows of test rows. Insecticides were not sprayed during the cropping period in order to maintain the natural whitefly population in the field. The MYMV disease incidence was recorded on all plants of F₂ populations and parents based on the visual scores on 60^th day after sowing. Based on disease grade two phenotypic classes were formed among F₂ plants with the scales of (1 to 3) as resistant phenotype and (4 to 9) as susceptible phenotype. Grouping of phenotypic classes were carried out as reported earlier (Dahiya et al., 1977; Verma and Singh, 1986; Singh, 1980; Dwivedi and Singh, 1985; Verma and Singh, 1986; Kaushal and Singh, 1988; Pal et al., 1991; Reddy and Singh 1995; Gupta et al., 2005; Murugan and Nadarajan, 2012). The rating scale suggested by Singh et al., (1988), was adopted as given below:
 
 
  
The goodness of fit to Mendelian segregation ratio for MYMV disease resistance in the segregating population was tested by Chi square test (Stansfield, 1991).

The details of parental particulars were presented in Table 1. Among eight crosses viz., MDU 1 × Mash 114, CO 5 × Mash 114, MDU 1 × VBN 6 and CO 5 × VBN 6 were resistant to MYMV disease, while other four crosses were found to be susceptible. The parents MDU 1 and CO 5 were used as common female parents for all the crosses. The appearance of both resistance and susceptibility in the F1s partly agreed with previous findings. Dominant nature of MYMV disease resistance was reported by Dahiya et al., (1977), Verma and Singh (1986), Kaushal and Singh (1988) and Murugan and Nadarajan (2012). While the recessive nature of MYMV disease resistance was reported by Singh (1980), Dwivedi and Singh (1985) and Verma and Singh (1986). The appearance of the various phenotypic expression of MYMV disease incidence among the F₁s clearly showed the contradiction on the inheritance pattern.

The inheritance patterns of MYMV disease resistance in F₂ generation of cross combinations were studied and the results are presented in Table 2. The results of the crosses viz., MDU 1 × Mash 114, CO 5 × Mash 114, MDU 1 × VBN 6 and CO 5 × VBN 6 indicated goodness of fit for trigenic inhibitory gene action for MYMV disease. These crosses had the common male parents viz., Mash 114 and VBN 6. The trigenic inheritance pattern indicated the presence of a third gene that influences the masking effect of phenotypic expression. Trigenic inhibitory gene action was reported by several workers in blackgram (Solanki et al., 1982; Verma and Singh, 1986; Reddy and Singh, 1995 and Murugan and Nadarajan, 2012). The results of crosses viz., MDU 1 x Mash 1008, CO 5 × Mash 1008, MDU 1 × VBN 8 and CO 5 × VBN 8 indicated goodness of fit for digenic complementary gene action for MYMV disease. These crosses had the male parents viz., Mash 1008 and VBN 8. A similar type of digenic interaction for MYMV resistance in black gram was reported by Verma and Singh (1980); Sandhu et al., (1985); Shukla and Pandiya (1985) and Thamodhran et al., (2015). The differential expression of the inheritance pattern showed that the variation might be due the alleic pattern of parents. The digenic nature of inheritance of MYMV disease can be explained only if the third gene is recessive in both parents of a cross. Based on these findings, putative gene symbols for each parent were worked out (Table 3). The female parents MDU1 and CO 5 had similar allelic pattern (S₁S₁S₂S₂ii), which act in complementation. Male parents Mash 114 and VBN 6 had similar allelic pattern (s₁s₁s₂s₂ii), in which third gene was responsible for the inhibitory gene action. Hence, the appearance of resistant phenotype in the F₁ (S₁s₁S₂s₂ii) might be due the influence of the inhibitory gene in the third locus. The male parents Mash 1008 and VBN 8 had similar allelic form (s₁s₁s₂s₂ii), and showed the complimentary gene interaction in the crosses. Hence the F₁ (S₁s₁S₂s₂ii) obtained from the cross combination involving male parents Mash 1008 and VBN 8 had susceptible reaction.





Based on the foregoing discussion, it may be concluded that the MYMV disease resistance is governed by recessive genes in these eight crosses of blackgram. The presence of three genes is confirmed with the various types of interaction obtained in the study. However, the gene symbols allotted are subject to confirmation by allelic tests. The allelic tests may be conducted by intercrossing all the four male parents and studied the resistant pattern for MYMV disease incidence. Hence, recombination breeding with two or three cycles of recurrent selection may be a viable option to harness the MYMV disease resistance in these two susceptible female parents of blackgram.