The nature of the resistance in groundnut to rosette disease

Groundnut rosette disease is caused by a complex of three agents, groundnut rosette virus (GRV) and its satellite RNA, and groundnut rosette assistor virus (GRAV); the satellite RNA is mainly responsible for the disease symptoms. Groundnut genotypes possessing resistance to rosette disease were shown to be highly resistant (though not immune) to GRV and therefore to its satellite RNA, but were fully susceptible to GRAV

Viruses associated with chlorotic rosette and green rosette diseases of groundnut in Nigeria

Groundnut (Arachis hypogaea) plants from Nigeria with chlorotic rosette disease contained a manually transmissible virus, considered to be a strain of groundnut rosette virus (GRV(C)). GRV(C) infected nine out of 32 species in three out of nine families. It caused local lesions without systemic infection in Chenopodium amaranticolor, C. murale and C. quinoa, and systemic symptoms in Glycine max, Nicotiana benthamiana, N. clevelandii and Phaseolus vulgaris as well as in groundnut. Some ‘rosette-resistant’ groundnut lines were also infected. GRV(C) was transmitted by Aphis craccivora, but only from groundnut plants that were also infected with an aphid-transmissible second virus, which was not manually transmissible and was considered to be groundnut rosette assistor virus (GRAV). Plants infected with GRAV contained isometric particles c. 25 nm in diameter which were detectable by immunosorbent electron microscopy on grids coated with antisera to several luteoviruses, especially with antisera to bean leaf roll, potato leafroll and beet western yellows viruses. No virus-like particles were observed in extracts from plants infected with GRV(C) alone. A single groundnut plant obtained from Nigeria with symptoms of green rosette contained luteovirus particles, presumed to be of GRAV, and yielded a manually transmissible virus that induced symptoms similar to those of GRV(C) in C. amaranticolor but gave only mild or symptomless infection of N. benthamiana and N. clevelandii. It was considered to be a strain of GRV and designated GRV(G)

Insulin-like growth factor-binding protein-2 promotes prostate cancer cell growth via IGF-dependent or -independent mechanisms and reduces the efficacy of docetaxel

Background: The development of androgen independence, chemo-, and radioresistance are critical markers of prostate cancer progression and the predominant reasons for its high mortality. Understanding the resistance to therapy could aid the development of more effective treatments. Aim: The aim of this study is to investigate the effects of insulin-like growth factor-binding protein-2 (IGFBP-2) on prostate cancer cell proliferation and its effects on the response to docetaxel. Methods: DU145 and PC3 cells were treated with IGFBP-2, insulin-like growth factor I (IGF-I) alone or in combination with blockade of the IGF-I receptor or integrin receptors. Cells were also treated with IGFBP-2 short interfering ribonucleic acid with or without a PTEN (phosphatase and tensin homologue deleted on chromosome 10) inhibitor or docetaxel. Tritiated thymidine incorporation was used to measure cell proliferation and Trypan blue cell counting for cell death. Levels of IGFBP-2 mRNA were measured using RT-PCR. Abundance and phosphorylation of proteins were assessed using western immunoblotting. Results: The IGFBP-2 promoted cell growth in both cell lines but with PC3 cells this was in an IGF-dependent manner, whereas with DU145 cells the effect was independent of IGF receptor activation. This IGF-independent effect of IGFBP-2 was mediated by interaction with β-1-containing integrins and a consequent increase in PTEN phosphorylation. We also determined that silencing IGFBP-2 in both cell lines increased the sensitivity of the cells to docetaxel. Conclusion: The IGFBP-2 has a key role in the growth of prostate cancer cells, and silencing IGFBP-2 expression reduced the resistance of these cells to docetaxel. Targeting IGFBP-2 may increase the efficacy of docetaxel.7 page(s

The moment protein (NSm) of Tomato spotted wilt virus is the avirulence determinant in the Sw-5 gene-based resistance

This is the accepted version of the following article: Peiró Morell, A.; Cañizares, MC.; Rubio, L.; López Del Rincón, C.; Moriones, E.; Aramburu, J.; Sanchez Navarro, JA. (2014). The moment protein (NSm) of Tomato spotted wilt virus is the avirulence determinant in the Sw-5 gene-based resistance. Molecular Plant Pathology. 15:802-813. doi:10.1111/mpp.12142., which has been published in final form at http://dx.doi.org/10.1111/mpp.12142 .The avirulence determinant triggering the resistance conferred by the tomato gene Sw-5 against Tomato spotted wilt virus (TSWV) is still unresolved. Sequence comparison showed two substitutions (C118Y and T120N) in the movement protein NSm present only in TSWV resistance-breaking (RB) isolates. In this work, transient expression of NSm of three TSWV isolates [RB1 (T120N), RB2 (C118Y) and non-resistance-breaking (NRB)] in Nicotiana benthamiana expressing Sw-5 showed a hypersensitive response (HR) only with NRB. Exchange of the movement protein of Alfalfa mosaic virus (AMV) with NSm supported cell-to-cell and systemic transport of the chimeric AMV RNAs into N.tabacum with or without Sw-5, except for the constructs with NBR when Sw-5 was expressed, although RB2 showed reduced cell-to-cell transport. Mutational analysis revealed that N120 was sufficient to avoid the HR, but the substitution V130I was required for systemic transport. Finally, co-inoculation of RB and NRB AMV chimeric constructs showed different prevalence of RB or NBR depending on the presence or absence of Sw-5. These results indicate that NSm is the avirulence determinant for Sw-5 resistance, and mutations C118Y and T120N are responsible for resistance breakdown and have a fitness penalty in the context of the heterologous AMV system.A.P. was a recipient of a JAE-Pre contract from the Consejo Superior de Investigaciones Cientificas (CSIC), and M. C. C was a recipient of an I3P contract from CSIC (co-financed by Fondo Social Europeo, FSE). We thank L. Corachan for excellent technical assistance and Dr Marcel Prins for providing the Nt/Sw5-b and Nb/Sw5-b seeds. This work was supported by grant BIO2011-25018 from the Spanish granting agency DGICYT, grant PAID05-11/2888 from the Universidad Politecnica de Valencia and by grant RTA2008-00010-C03 from the Instituto Nacional de Investigaciones Agrarias (INIA). All authors have no conflicts of interest to declare.Peiró Morell, A.; Cañizares, MDC.; Rubio, L.; López Del Rincón, C.; Moriones, E.; Aramburu, J.; Sanchez Navarro, JA. (2014). The moment protein (NSm) of Tomato spotted wilt virus is the avirulence determinant in the Sw-5 gene-based resistance. Molecular Plant Pathology. 15(8):802-813. https://doi.org/10.1111/mpp.12142S802813158Agudelo-Romero, P., de la Iglesia, F., & Elena, S. F. (2008). The pleiotropic cost of host-specialization in Tobacco etch potyvirus. 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Genetic Management of Virus Diseases in Peanut

Peanut, also known as groundnut (Arachis hypogaea L.) is a major oilseed crop in the world. About 31 viruses representing 14 genera are reported to naturally infe.ct peanut in different parts of the world, although only a few of these are of economic importance. These include groundnutrosette disease in Africa, tomato spotted wilt-disease in the United States, peanut bud necrosis disease in south Asia, and peanut stripe virus disease in east and southeast Asia. Cucumber mosaic virus disease in China and Argentina and peanut stem necrosis disease in certain -pockets in southern India are also economically important. Host plant resistance provides the most effective and economic option to manage virus diseases. However, for many virus diseases, effective resistance gene(s) in cultivated peanut have not been identified. With a few exceptions, the virus resistance breeding work has received little attention in peanut improvement programs. Transgenic resistance offers another option in virus resistance breeding. This review focuses on the status of genetic resistance to various economically important groundnut viruses and'use of transgenic-technology for the improvement of virus resistance