Mature plant and tissue resistance in the groundnut-peanut bud necrosis virus system

Leaves and plants of different ages of one susceptible (JL24) and two resistant (ICGV86031 and ICGV86388) groundnut genotypes were mechanically inoculated with peanut bud necrosis [tospo]virus, and the percentage of plants with systemic symptoms (incidence) and the incubation period were determined. The incidence decreased sharply in all three genotypes with the age of the inoculated leaves and plants. The incubation period increased with the age of leaves and plants. Apparently, only young tissue of young plants is susceptible, while mature tissue and plants are highly resistant. This mature tissue and plant resistance occurs irrespective of the susceptibility level of the genotype to peanut bud necrosis virus, however, it develops earlier in the resistant than in the susceptible genotype

Recent Studies on Peanut Bud Necrosis Disease: Proceedings of a Meeting 20 Mar 1995

The current status of research on peanut bud necrosis disease caused by the peanut bud necrosis virus and transmitted by Thrips palmi is reviewed. Recent advances in the genome structure, host range, transmission, and spread of tospoviruses wi t h emphasis on the peanut bud necrosis virus are discussed. Epidemiology of the disease and resistance to both the vector and the virus are reviewed in detail. Agronomically acceptable varieties wi th resistance to either the vector or to the vector and the virus are now available

Peanut Bud Necrosis Disease: An Overview

Peanut bud necrosis disease (PBND) was first recorded in India in 1949. The economic importance of the disease was realized during the late 1960s when incidences up to 100% were recorded in many groundnut-growing regions in India. The disease has been described under different names. It was shown to be economically important in parts of Tamil Nadu, Karnataka, Andhra Pradesh, Maharashtra, and Uttar Pradesh. Although it was earlier reported to be caused by tomato spotted wilt virus (TSWV), recently, the causal virus of PBND in India was shown to be a serologically distinct tospovirus, now referred to as peanut bud necrosis virus (PBNV), transmitted by Thrips palmi. Surveysin many groundnut-growing countries indicate that PBNV is restricted to South and Southeast Asia. Several cultural practices are available to control the disease. Excellent progress has been made in the identification of sources of field resistance. The PBNV genome contains three RNA species and the sRNA has recently been sequenced and the two genes it codes for have been identified. Progress achieved will lead to the production of high quality diagnostic aids and for the development of transgenic resistance. Future research will focus on epidemiology, development of early-maturingresistant cultivars, sequencing of the entire viral genome, the production of high quality diagnostic aids, and assessment of biodiversity among PBNV isolates

Genomic regions associated with resistance to peanut bud necrosis disease (PBND) in a recombinant inbred line (RIL) population

Parents and 318 F8 recombinant inbred lines (RILs) derived from the cross, TAG 24 × ICGV 86031 were evaluated for peanut bud necrosis disease (PBND) resistance and agronomic traits under natural infestation of thrips at a disease hotspot location for 2 years. Significant genotype, environment and genotype × environment interaction effects suggested role of environment in development and spread of the disease. Quantitative trait loci (QTL) analysis using QTL Cartographer identified a total of 14 QTL for six traits of which five QTL were for disease incidence. One quantitative trait locus q60DI located on LG_AhII was identified using both QTL Cartographer and QTL Network. Another QTL q90DI was detected with a high PVE of 12.57 using QTL Cartographer. A total of nine significant additive × additive (AA) interactions were detected for PBND disease incidence and yield traits with two and seven interactions displaying effects in favour of the parental and recombinant genotype combinations, respectively. This is the first attempt on QTL discovery associated with PBND resistance in peanut. Superior RILs identified in the study can be recycled or released as variety following further evaluations

Diagnosis and Resistance Breeding of Peanut Bud Necrosis Virus

he occurrence of peanut bud necrosis (PBN) disease in India was first reported in 1968. The high incidence of PBN disease during the 1960s coincided with large-scale imports of the peanut cultivars Asiria Mwitundae and Spanish Improved, both of which are highly susceptible to PBN. Since then, a number of reports have been published in India describing bud necrosis under at least seven different names (Reddy 1988). Crop losses due to PBN have been estimated at USD89 million per year in India during 1976–1986. The disease is also currently recognized as economically important in Nepal (Sharma 1996), in Sri Lanka, and in Thailand (Wongkaew 1995). The causal agent of PBN was originally reported as tomato spotted wilt virus (TSWV) (Ghanekar et al. 1979). Since then, methods to purify the causal virus of PBN have been developed, which facilitated the production of good quality antisera. On the basis of serological relationships, some physicochemical properties, and thrips transmission, it was shown that the causal virus of PBN in India was a distinct tospovirus that was named peanut bud necrosis virus (PBNV, Reddy et al. 1992). These results were subsequently confirmed by Adam et al. (1993). Later, monoclonal antibodies (MAbs) have been produced against the nucleocapsid (N) protein of PBNV (Poul et al. 1992). Antibodies from nine clones failed to react with a TSWV-lettuce (TSWV-L) isolate and with an impatiens necrotic spot virus (INSV) by triple-antibody sandwich enzyme-linked immunosorbent assay (TAS-ELISA) (coating of PBNV polyclonal antiserum, addition of antigen followed by addition of MAbs and antimouse IgGs conjugated to alkaline phosphatase). Of 16 MAbs produced against TSWV-L (Hsu et al. 1990), 12 H5 Al (f), 12 H5 H5 (