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Citrus miraculin-like protein hijacks a viral movement-related p33 protein and induces cellular oxidative stress in defence against Citrus tristeza virus.

ABSTRACT: To defend against pathogens, plants have developed a complex immune system, which recognizes the pathogen effectors and mounts defence responses. In this study, the p33 protein of Citrus tristeza virus (CTV), a viral membrane-associated effector, was used as a molecular bait to explore virus interactions with host immunity. We discovered that Citrus macrophylla miraculin-like protein 2 (CmMLP2), a member of the soybean Kunitz-type trypsin inhibitor family, targets the viral p33 protein. The expression of CmMLP2 was up-regulated by p33 in the citrus phloem-associated cells. Knock-down of the MLP2 expression in citrus plants resulted in a higher virus accumulation, while the overexpression of CmMLP2 reduced the infectivity of CTV in the plant hosts. Further investigation revealed that, on the one hand, binding of CmMLP2 interrupts the cellular distribution of p33 whose proper function is necessary for the effective virus movement throughout the host. On the other hand, the ability of CmMLP2 to reorganize the endomembrane system, amalgamating the endoplasmic reticulum and the Golgi apparatus, induces cellular stress and accumulation of the reactive oxygen species, which inhibits the replication of CTV. Altogether, our data suggest that CmMLP2 employs a two-way strategy in defence against CTV infection.

SUBMITTER: Sun YD

PROVIDER: S-EPMC8131049 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Citrus tristeza virus P33 Protein is Required for Efficient Transmission by the Aphid Aphis (Toxoptera) citricidus (Kirkaldy).

Project description:Plant viruses are threatening many valuable crops, and Citrus tristeza virus (CTV) is considered one of the most economically important plant viruses. CTV has destroyed millions of citrus trees in many regions of the world. Consequently, understanding of the transmission mechanism of CTV by its main vector, the brown citrus aphid, Aphis (Toxoptera) citricidus (Kirkaldy), may lead to better control strategies for CTV. The objective of this study was to understand the CTV-vector relationship by exploring the influence of viral genetic diversity on virus transmission. We built several infectious clones with different 5'-proximal ends from different CTV strains and assessed their transmission by the brown citrus aphid. Replacement of the 5'- end of the T36 isolate with that of the T30 strain (poorly transmitted) did not increase the transmission rate of T36, whereas replacement with that of the T68-1 isolate (highly transmitted) increased the transmission rate of T36 from 1.5 to 23%. Finally, substitution of p33 gene of the T36 strain with that of T68 increased the transmission rate from 1.5% to 17.8%. Although the underlying mechanisms that regulate the CTV transmission process by aphids have been explored in many ways, the roles of specific viral proteins are still not explicit. Our findings will improve our understanding of the transmission mechanisms of CTV by its aphid vector and may lead to the development of control strategies that interfere with its transmission by vector.

| S-EPMC7600554 | biostudies-literature

The p23 of Citrus Tristeza Virus Interacts with Host FKBP-Type Peptidyl-Prolylcis-Trans Isomerase 17-2 and Is Involved in the Intracellular Movement of the Viral Coat Protein.

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| S-EPMC8073322 | biostudies-literature

Autophagy Inhibits Intercellular Transport of Citrus Leaf Blotch Virus by Targeting Viral Movement Protein.

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| S-EPMC8619118 | biostudies-literature

High codon adaptation in citrus tristeza virus to its citrus host.

Project description:BackgroundCitrus tristeza virus (CTV), a member of the genus Closterovirus within the family Closteroviridae, is the causal agent of citrus tristeza disease. Previous studies revealed that the negative selection, RNA recombination and gene flow were the most important forces that drove CTV evolution. However, the CTV codon usage was not studied and thus its role in CTV evolution remains unknown.ResultsA detailed comparative analysis of CTV codon usage pattern was done in this study. Results of the study show that although in general CTV does not have a high degree of codon usage bias, the codon usage of CTV has a high level of resemblance to its host codon usage. In addition, our data indicate that the codon usage resemblance is only observed for the woody plant-infecting closteroviruses but not the closteroviruses infecting the herbaceous host plants, suggesting the existence of different virus-host interactions between the herbaceous plant-infecting and woody plant-infecting closteroviruses.ConclusionBased on the results, we suggest that in addition to RNA recombination, negative selection and gene flow, host plant codon usage selection can also affect CTV evolution.

| S-EPMC3416656 | biostudies-literature

The Intriguing Conundrum of a Nonconserved Multifunctional Protein of Citrus Tristeza Virus That Interacts with a Viral Long Non-Coding RNA.

Project description:Citrus tristeza virus (CTV), the largest non-segmented plant RNA virus, has several peculiar features, among which is the production of a 5'-terminal long non-coding RNA (lncRNA) termed low-molecular-weight tristeza 1 (LMT1). In this study, we found that p33, a unique viral protein that performs multiple functions in the virus infection cycle, specifically binds LMT1, both in vivo and in vitro. These results were obtained through the expression of p33 under the context of the wild type virus infection or along with a mutant CTV variant that does not produce LMT1 as well as via ectopic co-expression of p33 with LMT1 in Nicotiana benthamiana leaves followed by RNA immunoprecipitation and rapid amplification of cDNA ends assays. Further experiments in which a recombinant p33 protein and an in vitro transcribed full-length LMT1 RNA or its truncated fragments were subjected to an electrophoretic mobility shift assay demonstrated that p33 binds to at least two distinct regions within LMT1. To the best of our knowledge, this is the first report of a plant virus protein binding to a lncRNA produced by the same virus. The biological significance of the interaction between these two viral factors is discussed.

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The resistance of sour orange to Citrus tristeza virus is mediated by both the salicylic acid and RNA silencing defence pathways.

Project description:Citrus tristeza virus (CTV) induces in the field the decline and death of citrus varieties grafted on sour orange (SO) rootstock, which has forced the use of alternative decline-tolerant rootstocks in affected countries, despite the highly desirable agronomic features of the SO rootstock. Declining citrus plants display phloem necrosis below the bud union. In addition, SO is minimally susceptible to CTV compared with other citrus varieties, suggesting partial resistance of SO to CTV. Here, by silencing different citrus genes with a Citrus leaf blotch virus-based vector, we have examined the implication of the RNA silencing and salicylic acid (SA) defence pathways in the resistance of SO to CTV. Silencing of the genes RDR1, NPR1 and DCL2/DCL4, associated with these defence pathways, enhanced virus spread and accumulation in SO plants in comparison with non-silenced controls, whereas silencing of the genes NPR3/NPR4, associated with the hypersensitive response, produced a slight decrease in CTV accumulation and reduced stunting of SO grafted on CTV-infected rough lemon plants. We also found that the CTV RNA silencing suppressors p20 and p23 also suppress the SA signalling defence, with the suppressor activity being higher in the most virulent isolates.

| S-EPMC6638288 | biostudies-literature

Plant Viral Movement Protein-expressing Yeast Transcriptome compared with Non-Functional Plant Viral Movement Protein-expressing Yeast Transcriptome

Project description:Virus life cycle heavily depends on their ability to command the host machinery in order to translate their genomes. By using a yeast-based approach we have found that over expression of the PNRSV MP caused a severe growth defect in yeast cells. cDNA microarrays analysis carried out to characterise at the molecular level the growth interference phenotype reported the induction of genes related to amino acid deprivation suggesting that expression of MP activates the GCN pathway in yeast cells. Yeast cell cultures were grown 24h in minimal medium with doxycycline (100 mg/ml). These cultures were then diluted to an OD600 nm of 0.1 into fresh minimal medium without doxycycline. At 6 h total RNA was extracted from yeast cells transformed with the pCM:MPpnrsv and MPpnrsvΔHR, a non-functional MPpnrsv mutant lacking its hydrophobic region.

2011-12-01 | E-GEOD-26120 | biostudies-arrayexpress

High incidence of citrus tristeza virus in mandarin (Citrus reticulata) in North-East states of India.

Project description:Khasi mandarin is one of the most remunerative crop in North Eastern Hills region of India playing a very critical role in the socio-economic upliftment of the people. The orchards of this region were found to express the typical symptoms of citrus tristeza virus (CTV). An extensive survey of the Khasi mandarin orchard for six North Eastern states of India namely Arunachal Pradesh, Meghalaya, Assam, Nagaland, Sikkim and Tripura, was carried out to establish the identity of these viruses using ELISA and PCR/RT-PCR techniques. Out of 300 Khasi mandarin tree samples collected from the six states, 172 were found to be positive for CTV infection by DAS-ELISA indicating 57.33% overall CTV disease incidence. Results revealed presence of CTV in all the surveyed states showing a maximum incidence of 66.00% in Arunachal Pradesh followed by 62.00% in Assam, 60.00% in Meghalaya and Nagaland, 54.00% in Sikkim and 42.33% in Tripura. Higher CTV concentration was recorded in the age group > 15 years (69.09%) followed by 10-15 (57%) and 5-10 years (43.33%). However, this study, to the best of our knowledge, is the first report for the detection of CTV in Khasi mandarin from Arunachal Pradesh, Nagaland and Tripura and also the first authentic survey of overall disease incidence of CTV Khasi mandarins from the six major mandarin growing North Eastern states of India.

| S-EPMC5747839 | biostudies-other

Plant Viral Movement Protein-expressing Yeast Transcriptome compared with Non-Functional Plant Viral Movement Protein-expressing Yeast Transcriptome

2011-12-01 | GSE26120 | GEO

Minor Variants of Orf1a, p33, and p23 Genes of VT Strain Citrus Tristeza Virus Isolates Show Symptomless Reactions on Sour Orange and Prevent Superinfection of Severe VT Isolates.

Project description:The control of tristeza quick decline (QD) of citrus is based on the use of rootstocks that are tolerant or resistant to the Citrus tristeza virus (CTV), but some of them show bio-agronomic limits. The application of cross-protection (CP) has been insufficiently explored. The present study examined the possibility of QD control by cross-protection (CP) following reports showing the dependence of the CP strategy on the close genetic relationships between the protective and challenging CTV isolates. Taking advantage of deep sequencing technologies, we located six naturally infected trees harboring no-seedling yellow (no-SY) and no QD decline (mild) VT isolates and used these for challenge inoculation with three QD VT isolates. Symptom monitoring showed that all six Sicilian mild no-SY isolates, based on their genomic relatedness and mild symptoms reactions, provide effective protection against the three severe local VT isolates. The differences between the six mild and three severe isolates were confined to just a few nucleotide variations conserved in eight positions of three CTV genes (p23, p33, and Orf1a). These results confirm that the superinfection exclusion (SIE mechanism) depends on close genetic relatedness between the protective and challenging severe VT strain isolates. Ten years of investigation suggest that CP could turn into an efficient strategy to contain CTV QD infections of sweet orange trees on SO rootstock.

| S-EPMC10612028 | biostudies-literature

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