Plants have evolved diverse mechanism to recognize pathogen attack and triggers defense responses. These defense responses alter host cellular function regulated by endogenous, small, non-coding miRNAs. To understand the mechanism of miRNAs regulated cellular functions during stem rust infection in wheat, we investigated eight different miRNAs viz. miR159, miR164, miR167, miR171, miR444, miR408, miR1129 and miR1138, involved in three different independent cellular defense response to infection. The investigation reveals that at the initiation of disease, accumulation of miRNAs might be playing a key role in hypersensitive response (HR) from host, which diminishes at the maturation stage. This suggests a possible host-fungal synergistic relation leading to susceptibility. Differential expression of these miRNAs in presence and absence of R gene provides a probable explanation of miRNA regulated R gene mediated independent pathways.
Background: Groundnut bud necrosis virus (GBNV) (Tospovirus genus, Bunyaviridae family) infects the major crops of solanaceae, leguminosae and cucurbitaceae in India. Temperature is an important factor which influences the plant growth and development under diseased conditions. Objective: In the present study, we evaluated the effect of four different temperatures on the symptoms expression and viral RNA accumulation in the GBNV inoculated cowpea plants. Material and Methods: For the evaluation of viral symptoms and RNA accumulation, we used 2-3 leaf stage cowpea plants grown in the controlled conditions. GBNV was mechanically inoculated by sap method to the cowpea plants and inoculated plants were incubated at four different temperatures (30, 25, 20 and 15 °C). Results: The first visible symptom of GBNV infection at the inoculated site was observed in the form of chlorotic spots which were converted into the necrotic spots as the infections succeeded. Some yellow mosaic symptoms were also observed at the systemic site during viral infection cycle. Plants incubated at higher (30 and 25 °C) temperatures showed a severe necrosis and a higher viral RNA accumulation at the inoculated site and facilitated the viral spread at the systemic site. However, viral RNA accumulation was less at the systemic site than the inoculated site. In contrast, symptoms' expression and viral RNA accumulation were decreased at the inoculated site at low (20 and 15 °C) temperatures, no viral symptoms were observed at the systemic site (15 °C); in addition to viral RNA accumulation suppression at this site. GBNV infection at the inoculated site induced the higher accumulation of H 2 O 2 followed by the induction of cell death at higher temperatures (30 and 25 °C) than the lower (20 and 15 °C) temperatures. Conclusion: This study suggests that viral RNA accumulation parallels with the H 2 O 2 production and induction of cell death by GBNV infection in cowpea plants is temperature dependent.
Groundnut bud necrosis virus induces necrotic symptoms in different hosts. Previous studies showed reactive oxygen species-mediated programmed cell death (PCD) resulted in necrotic symptoms. Transgenic expression of viral protein NSs mimics viral symptoms. Here, we showed a role for NSs in influencing oxidative burst in the cell, by analyzing HO accumulation, activities of antioxidant enzymes and expression levels of vacuolar processing enzymes, HO-responsive microRNA 319a.2 plus its possible target metacaspase-8. The role of NSs in PCD, was shown using two NSs mutants: one in the Trp/GH3 motif (a homologue of pro-apototic domain) (NSs) and the other in a non-Trp/GH3 motif (NSs). Tobacco rattle virus (TRV) expressing NSs enhanced the PCD response, but not TRV-NSs, while RNA silencing suppression activity was lost in TRV-NSs, but not in TRV-NSs. Therefore, we propose dual roles of NSs in RNA silencing suppression and induction of cell death, controlled by different motifs.
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