Legume Research

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Legume Research, volume 46 iussue 5 (may 2023) : 660-663

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

K. Vadivel1, N. Manivannan2,*, A. Mahalingam3, V.K. Satya4, S. Ragul2
1National Pulses Research Center, Tamil Nadu Agricultural University, Vamban-622 303, Tamil Nadu, India.
2Centre of Excellence in Molecular Breeding, Tamil Nadu Agricultural University, Coimbatore-641 003, Tamil Nadu, India.
3Regional Research Station, Tamil Nadu Agricultural University, Virudhachalam-606 001, Tamil Nadu, India.
4Anbil Dharmalingam Agricultural College and Research Institute, Tamil Nadu Agricultural University, Trichy-620 009, Tamil Nadu, India.
  • Submitted11-06-2020|

  • Accepted24-04-2021|

  • First Online 08-05-2021|

  • doi 10.18805/LR-4439

Cite article:- Vadivel K., Manivannan N., Mahalingam A., Satya V.K., Ragul S. (2023). Inheritance Pattern of Mungbean Yellow Mosaic Virus (MYMV) Disease Resistance in Blackgram [Vigna mungo (L.) Hepper] . Legume Research. 46(5): 660-663. doi: 10.18805/LR-4439.
Background: Mungbean yellow mosaic virus (MYMV) disease is the most destructive disease in blackgram. Development of MYMV resistant varieties is one of the best possible solutions to avoid the yield reduction in blackgram. There are conflicting reports on the genetics of resistance to MYMV disease claiming that it is controlled by both dominant and recessive genes. Hence the present study was aimed to understand the inheritance pattern of the MYMV disease resistance in eight crosses of blackgram.

Methods: Parents, F1 and F2 generation of eight cross combinations were raised during July - Sep, 2018 at National Pulses Research Centre, Tamil Nadu Agricultural University, Vamban, Tamil Nadu. An infector row of CO 5 was raised to intensify the MYMV disease pressure after every eight rows. Based on disease incidence on 60th day after sowing, 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. The goodness of fit to Mendelian segregation ratio for MYMV disease resistance in the segregating population was tested by Chi square test (Stansfield, 1991).

Result: The MYMV disease incidence was tri-genically controlled with inhibitory gene action in four crosses viz., MDU 1 x Mash 114, CO5 x Mash 114, MDU 1 x VBN 6 and CO 5 x VBN 6. Complementary gene action with two genes was observed in four crosses viz., MDU 1 x Mash 1008, CO 5 x Mash 1008, MDU 1 x VBN 8 and CO 5 x VBN 8. Differences in number of genes were observed due to the presence of recessive inhibitory gene in both male and female parents of the crosses which had complementary gene action for MYMV disease. The putative gene symbols assigned for the six genotypes viz., S1S1S2S2ii (MDU 1 and CO 5), s1s1s2s2II (Mash 114 and VBN 6) and s1s1s2s2ii (Mash 1008 and VBN 8), respectively. 
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 60th 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.

Table 2: Chi-square test for inheritance of MYMV disease resistance in blackgram.



Table 3: Gene symbols for parents involved in the study.



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.

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