The six Tomato yellow leaf curl virus genes expressed individually in tomato induce different levels of plant stress response attenuation

Abstract

Tomato yellow leaf curl virus (TYLCV) is a begomovirus infecting tomato plants worldwide. TYLCV needs a healthy host environment to ensure a successful infection cycle for long periods. Hence, TYLCV restrains its destructive effect and induces neither a hypersensitive response nor cell death in infected tomatoes. On the contrary, TYLCV counteracts cell death induced by other factors, such as inactivation of HSP90 functionality. Suppression of plant death is associated with the inhibition of the ubiquitin 26S proteasome degradation and with a deactivation of the heat shock transcription factor HSFA2 pathways (including decreased HSP17 levels). The goal of the current study was to find if the individual TYLCV genes were capable of suppressing HSP90-dependent death and HSFA2 deactivation. The expression of C2 (C3 and CP to a lesser extent) caused a decrease in the severity of death phenotypes, while the expression of V2 (C1 and C4 to a lesser extent) strengthened cell death. However, C2 or V2 markedly affected stress response under conditions of viral infection. The downregulation of HSFA2 signaling, initiated by the expression of C1 and V2, was detected in the absence of virus infection, but was enhanced in infected plants, while CP and C4 mitigated HSFA2 levels only in the infected tomatoes. The dependence of analyzed plant stress response suppression on the interaction of the expressed genes with the environment created by the whole virus infection was more pronounced than on the expression of individual TYLCV genes.

Heat Shock Proteins: Dynamic Biomolecules to Counter Plant Biotic and Abiotic Stresses

“…Silencing of HSP70 in the tomato plant controlled the viral infection. Conversely, HSP90 knockdown promoted viral infection [10,111]. A recent study on Potato Virus Y (PVY) in potato thermo-tolerant and sensitive genotypes under heat stress, HSPs was induced in both genotypes.…”

“…Plants continuously confront harsh environments like high/low temperatures, drought, salts, heavy metals, light, flooding and physical wounding [2,3,4,5]. Biotic stresses like pathogens (Viruses, Bacteria, Fungi) and pests such as nematodes, insects, and rodents also restrict plant productivity [6,7,8,9,10]. Negative effects of these stresses on the plant germination [11], are stunted growth [12,13], sunburn and scorching of leaves [14], loss of photosynthetic pigment, decreased production of photo-assimilates, and depletion of carbohydrate reserves which results in starvation [15,16,17,18].…”

Tomato yellow leaf curl virus intergenic siRNAs target a host long noncoding RNA to modulate disease symptoms

“…In addition, V2 is shown to affect host cell death by interacting with and inhibiting enzymatic activity of CYP1, a plant programmed cell death machinery component [11]. A recent report showed that overexpression of V2 induced cell death symptoms in tomato, in contrast to no cell death caused by TYLCV infection [12]. But a healthy environment ensures the survival and multiplication of TYLCV, so the accumulation of TYLCV was hindered at the late stages of infection [12].…”

“…A recent report showed that overexpression of V2 induced cell death symptoms in tomato, in contrast to no cell death caused by TYLCV infection [12]. But a healthy environment ensures the survival and multiplication of TYLCV, so the accumulation of TYLCV was hindered at the late stages of infection [12]. These results suggest that the individual viral proteins are insufficient to account for the TYLCV disease symptoms and other viral factor(s) may also contribute to the pathogenesis of the virus.…”

The Spread and Transmission of Sweet Potato Virus Disease (SPVD) and Its Effect on the Gene Expression Profile in Sweet Potato

“…To elucidate sweet potato's defense response against SPVD and to discover potential SPVD resistance mechanisms, we explored DEGs related to plant-pathogen interaction and defense response. Homologs of heat shock protein 70 (HSP70) and heat shock protein 90 (HSP90) genes, which have been reported to play key roles in resistance to viruses in plants [23][24][25], were significantly induced in SPFMV and SPCSV-infected sweet potato. The RPM1-interacting protein 4 (RIN4) gene homolog was also upregulated, as were unigenes encoding WRKY1, WRKY6, WRKY22, and WRKY40-like WRKY transcriptional factors.…”