The whitefly (Bemisia tabaci Gennadius) transmitted Tomato yellow leaf curl virus (TYLCV) disease is a limiting factor in tomato production. Breeding resistance into tomatoes is one of the options to manage the disease. Among various screening techniques available for TYLCV, whitefly mediated individual plant inoculation technique is the most reliable one. Till date, six independently inherited major resistance genes and few Quantitative Trait Loci (QTLs) have been mapped in wild tomato species including S. chilense (Ty-1, Ty-3, Ty-4 and Ty-6), S. habrochaites syn. L. hirsutum (Ty-2), and S. peruvianum (ty-5). Ty-1 and Ty-2 genes express complete or nearly complete dominance, while Ty-3 shows partial dominance. These three genes have been extensively used in resistance breeding programs to combat both the monopartite and the bipartite begomoviruses. Since the Ty-genes in general exhibit partial or incomplete dominance, single gene F1 hybrids are less effective than the pure lines homozygous for the resistance gene. Therefore, for hybrids to be effective either both the parents should be resistant or they involve multiple resistance genes. In this review, we have compiled up-to-date information on TYLCV occurrence and pathogen variability, allele mining, genetic mapping and cultivar development; and visualised future prospects of TYLCV resistance breeding in tomato.
Whitefly Bemisia tabaci is a global invasive pest that causes substantial losses to agricultural crops worldwide either by direct feeding or vectoring numerous plant viruses. Management with insecticides remains a big challenge due to its rapid resistance development potential as well as the impact of these chemicals on non-target organisms. Thus, in search of alternate and novel pest management strategies RNA interference (RNAi) has come up as potential future tool in this direction. The present study targets nine potential genes (Aquaporin (AQP), Calcitonin (CAL), CyclophilinB (CYCP), Knottin-1 (k-1), Heat shock proteins (Hsp20, Hsp40 and Hsp70), SWItch/Sucrose Non-fermentable (SNF7) and inhibitor of apoptosis (IAP) of whitefly that have been implicated to play a role in various vital physiological functions and virus transmission. The RNAi mediated knockdown efficiency of these genes has been improved through the conjugation of respective target gene dsRNA with CQD (carbon quantum dots) nanoparticles or simultaneous knockdown of dsRNA specific gut nucleases. The studies revealed that feeding of dsRNA (40 μg/ml sucrose diet) of the target gene(s) either conjugated with CQD or along with dsRNA against dsRNase (dsdsRNase) (40 μg/ml sucrose diet) enhanced the RNAi efficiency by 24–89% compared to whiteflies fed with naked dsRNA of the same target gene. The studies provide insights about the functional role of various genes in whitefly, which can possibly be exploited for the management of this pest in the future.
Yellow mosaic disease (YMD) in bitter gourd (Momordica charantia) is a devastating disease that seriously affects its yield. Although there is currently no effective method to control the disease, breeding of resistant varieties is the most effective and economic option. Moreover, quantitative trait locus (QTL) associated with resistance to YMD has not yet been reported. With the objective of mapping YMD resistance in bitter gourd, the susceptible parent “Punjab-14” and the resistant parent “PAUBG-6” were crossed to obtain F4 mapping population comprising 101 individuals. In the present study, the genotyping by sequencing (GBS) approach was used to develop the genetic linkage map. The map contained 3,144 single nucleotide polymorphism (SNP) markers, consisted of 15 linkage groups, and it spanned 2415.2 cM with an average marker distance of 0.7 cM. By adopting the artificial and field inoculation techniques, F4:5 individuals were phenotyped for disease resistance in Nethouse (2019), Rainy (2019), and Spring season (2020). The QTL analysis using the genetic map and phenotyping data identified three QTLs qYMD.pau_3.1, qYMD.pau_4.1, and qYMD.pau_5.1 on chromosome 3, 4, and 5 respectively. Among these, qYMD.pau_3.1, qYMD.pau_4.1 QTLs were identified during the rainy season, explaining the 13.5 and 21.6% phenotypic variance respectively, whereas, during the spring season, qYMD.pau_4.1 and qYMD.pau_5.1 QTLs were observed with 17.5 and 22.1% phenotypic variance respectively. Only one QTL qYMD.pau_5.1 was identified for disease resistance under nethouse conditions with 15.6% phenotypic variance. To our knowledge, this is the first report on the identification of QTLs associated with YMD resistance in bitter gourd using SNP markers. The information generated in this study is very useful in the future for fine-mapping and marker-assisted selection for disease resistance.