Strains Of Turnip Mosaic Virus Research Articles

Turnip Mosaic Virus Strains in Cruciferous Hosts in Taiwan

Turnip Mosaic Virus Strains in Cruciferous Hosts in Taiwan

A Destructive Disease of Garden Balsam Caused by a Strain of Turnip Mosaic Virus

A Destructive Disease of Garden Balsam Caused by a Strain of Turnip Mosaic Virus

Effects of infection with the cabbage black ringspot strain of turnip mosaic virus on turnip as a host to Myzus persicae and Brevicoryne brassicae

SUMMARYWhen turnip plants with 3–7 leaves were inoculated with cabbage black ringspot virus (CBRSV) on the 3rd rough‐leaf, symptoms only appeared on leaves that had been less than 15 mm long at the time of inoculation, although infection decreased the area and both fresh and dry weight of all leaves. Leaves were ‘aged’ by their appearance and placed in Leaf Age Categories (LACs). Leaves with symptoms senesced (‘aged’) prematurely.CBRSV‐infection of cv. Green Top White did not change the distribution of populations of Myzus persicae between LACs, but increased the proportion of the plant suitable for colonisation. All suitable LACs were quickly colonised by adult apterae and nymphs. On CBRSV‐infected plants the nymphal period was shorter, F1 adults deposited larvae more frequently and the live body weight and tibial length of the F2 generation was greater, than on healthy plants.The distribution of Brevicoryne brassicae populations on cv. Green Top White differed from that of M. persicae but was also unchanged by CBRSV‐infection. On healthy plants the largest colonies were on mature leaves, so that on virus‐infected plants premature senescence shortened the life of the colony. On CBRSV‐infected plants the nymphal period was prolonged and the live weight of F1 and F2 adult apterae was less than on healthy plants. The differences between the biology of M. persicae and B. brassicae on CBRSV‐infected cv. Green Top White were associated with the accelerated senescence of CBRSV‐infected leaves.The possibility that CBRSV‐infection might reduce the resistance of turnips to aphid infestation was tested. M. persicae and B. brassicae were cultured on two favourable and two less favourable cultivars. No improvement in population growth rate was found when the less favourable host cultivars were infected with CBRSV, but both aphid species weighed less and/or had smaller nymphal populations on cultivars showing the severest symptoms. These results are discussed in relation to the evolution of non‐persistent virus transmission by aphids.

Evaluation of Chinese Cabbage Cultivars from Japan and the People's Republic of China for Resistance to Turnip Mosaic Virus and Cauliflower Mosaic Virus1

Abstract In greenhouse and field tests, 46 accessions of Chinese cabbage (Brassica campestris L. ssp. pekinensis (Lour.) Olsson), recently introduced from Japan and the People's Republic of China (PRC), were evaluated for resistance to 3 major strains of turnip mosaic virus (TuMV-Cl, TuMV-C2, and TuMV-C3) and one of cauliflower mosaic virus (CaMV-1). Immunity and/or resistance to the TuMV strains was found among Chinese plant introductions (PI), whereas in Japanese cultivars sources of immunity or resistance were confined to the strains TuMV-C1 and TuMV-C2. None of the 46 cultivars was resistant to CaMV-1. PI 391560(1), PI 418957, PI 418959, and PI 419069 from the PRC were immune or resistant to each of the 3 strains of TuMV, representing valuable germplasm material for intra- and interspecific gene transfer. In early fall of 1979, an isolate of TuMV was recovered from a systemically infected plant of PI 391560(1). Although uncommon, resistance to this newly recognized strain (TuMV-C4) was found in plants of PI 418957. Strain specificity must be considered in developing TuMV-resistant cultivars, since their performance will depend upon the presence and distribution of the virus strains in a given locality.

Biological and Serological Characterization of the Alliaria Strain of Turnip Mosaic Virus

Journal of PhytopathologyVolume 86, Issue 1 p. 90-96 Biological and Serological Characterization of the Alliaria Strain of Turnip Mosaic Virus Vittoria Lisa, Corresponding Author Vittoria Lisa Laboratorio di Fitovirologia applicata del Consiglio Nazionale delle Ricerche — Torino, ItalyAuthors' address: Laboratorio di Fitovirologia applicata del CNR, Via O. Vigliani 104, I-10135 Torino (Italy).Search for more papers by this authorO. Lovisolo, Corresponding Author O. Lovisolo Laboratorio di Fitovirologia applicata del Consiglio Nazionale delle Ricerche — Torino, ItalyAuthors' address: Laboratorio di Fitovirologia applicata del CNR, Via O. Vigliani 104, I-10135 Torino (Italy).Search for more papers by this author Vittoria Lisa, Corresponding Author Vittoria Lisa Laboratorio di Fitovirologia applicata del Consiglio Nazionale delle Ricerche — Torino, ItalyAuthors' address: Laboratorio di Fitovirologia applicata del CNR, Via O. Vigliani 104, I-10135 Torino (Italy).Search for more papers by this authorO. Lovisolo, Corresponding Author O. Lovisolo Laboratorio di Fitovirologia applicata del Consiglio Nazionale delle Ricerche — Torino, ItalyAuthors' address: Laboratorio di Fitovirologia applicata del CNR, Via O. Vigliani 104, I-10135 Torino (Italy).Search for more papers by this author First published: May 1976 https://doi.org/10.1111/j.1439-0434.1976.tb04658.xCitations: 11 With 4 figures AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Citing Literature Volume86, Issue1May 1976Pages 90-96 RelatedInformation

The Coat Protein of the Alliaria Strain of Turnip Mosaic Virus: Molecular Weight and Degradation Products Formed During Purification and Upon Storage

SUMMARY Protein obtained by degradation of particles of the ‘Alliaria’ strain of TuMV (AlTuMV) was heterogeneous. Polyacrylamide gel electrophoresis experiments showed that this heterogeneity is greatly increased when purified virus suspensions are stored for 60 h in 0.02 m-borate buffer, pH 7.5, at 4 °C instead of being immediately degraded with 1% sodium dodecyl sulphate (SDS). When freshly purified virus particles were degraded, the protein preparations contained three components, I, II and III (estimated mol. wt. 38000, 30000 and 27500, respectively) whose relative amounts differed between samples of virus. It is suggested that components II and III, which both react against AlTuMV antiserum, are produced by degradation of component I. Electrophoresis in the presence of urea at different gel concentrations indicated that components I, II and III observed in the polyacrylamide-SDS system differ both in mol. wt. and in charge density.

Characterization of the capsid and cylindrical inclusion proteins of three strains of turnip mosaic virus

Three isolates of turnip mosaic virus (TuMV) from turnip (TuMV-T), rutabaga (TuMV-R), and Dames violet (TuMV-D) were determined to be distinct strains on the bases of the serological properties of their capsid proteins and the morphological properties of their cylindrical inclusions. Ouchterlony double-diffusion tests showed that the sodium dodecyl sulfate (SDS)-dissociated capsid of TuMV-D was antigenically distinct from those of TuMV-T and TuMV-R. Negative staining and thin sectioning of the virus-induced cylindrical inclusions in isolated preparations and in situ, respectively, showed that the cylindrical inclusions induced by TuMV-R were morphologically distinct from those induced by TuMV-T and TuMV-D. The SDS-dissociated capsid and cylindrical inclusion subunits showed similar electrophoretic mobilities in polyacrylamide gels and no antigenic differences were noted between the SDS-dissociated cylindrical inclusions.

Translocation of Necrotic Lesions within Virus Diseased Local Lesion Hosts

1) Daikon mosaic virus (DMV: the Japanese strain of turnip mosaic virus) and tobacco mosaic virus (TMV) were sap inoculated on leaves of Chenopodium album or of C. amaranticolor plants. Ten to thirty days after inoculation, several necrotic spots which have no connection with the primary local lesions on the inoculated leaves were produced abruptly on upper young leaves. These necrotic spots were tentatively called “translocated necrotic Lesions” (TNLs, Fig. 1 and 3). In the case of Chenopodium plants, daily production of TNLs gradually decreased in number, and sixty to hundred days after inoculation TNL formation stopped completely.It was found that no TNL was produced on meristematic tissues of stem apices and also on mature leaves.From TNLs the viruses were recovered easily, while attempts to recover the viruses from non-necrotic portions of the same leaves were unsuccessful. Moreover, the leaf with TNLs showed no cross protection reaction against challenge inoculation of the same virus (Fig. 2).2) Local lesion hosts of tobacco mosaic virus-tomato strain (TMV-T), Nicotiana sylvestris or N. glutinosa plants were grafted with N. tabacum var. Xanthi, a systemic (mosaic) host of the virus strain. One to two months after grafting, the virus was inoculated on leaves of the Xanthi part of the grafted plant. Forty to sixty days after inoculation of the virus, TNLs were produced abruptly on young leaves of the necrotic lesion hosts slightly below the stem apex (Fig. 4 and Fig. 5). In the case of N. sylvestris plants, TNLs were frequently produced on midribs.Unlike the case of Chenopodium plants, TNLs on young leaves near the stem apex of Nicotiana plants increased gradually in number and also enlarged themselves throughout the stem apex. The necrotic portions then extended downwards, and resulted finally in the death of the whole shoots of the necrotic hosts.Recovery of the inoculated virus from TNLs on Nicotiana plants was successful, while from the leaf portion outside of TNLs it was unsuccessful. Moreover, no cross protection reaction of the non-necrotic portions of the leaf against challenge inoculation of the same virus was observed.3) The mechanisms of TNL formation and the cause of the regularity of TNL distribution within the shoot of necrotic host plants have been explained, according to the hypothesis of “transcription of viral code by the host cell” reported elsewhere43) as follows:The viral code carried by double stranded TMV-RNA is translocated from the primary necrotic lesions to the growing tissues of young shoots via sieve tube. When the code is transferred to a young cell having nucleus so far grown to be able to transcribe the viral code, the cell will reproduce the virus. When the code-carrying double stranded RNA is translocated into a mature cell of the necrotic host, the carrier will soon be degraded within the cytoplasm. Thus regularity in distribution of the translocated necrotic lesions on the affected shoots ensues.

A quasi-genetic model for plant virus host ranges: III. Congruence and relatedness

Host-range containment occurs when all tested species susceptible to one virus are susceptible to a second virus, and the second virus can infect other species that the first one can not. This condition was found to be the extreme of a frequent tendency toward congruence of experimental host ranges, whether the tested viruses were related or not. The tendency arose partly from the general susceptibility of some taxonomic groups to a number of viruses and the relative insusceptibility of other groups, but it was mainly characteristic of the viruses and their origins. Statistical examination of the reactions of many plant species, each inoculated with 2 viruses, revealed degrees of congruence between some virus host ranges, and no congruence between others. Among strains of turnip mosaic virus (TuMV) were examples of host range containment extending to symptom types as well as susceptibility, and serial containment and divergence of host ranges, which possibly indicated short-range evolutionary trends. The type and intensity of symptoms produced in a group of 5 related Brassica species by 6 strains of TuMV were tabulated as a containment series. The contraction in host ranges was paralleled by a significant diminution of symptom intensity. The parallelism did not apply to strains outside the containment series. The facts revealed in this study were fitted into a quasi-genetic model already suggested for the determination of plant virus host ranges.

Inhibitory Effect of Chenopodium Sap on Virus Infection

Chenopodium sap used mainly in this study was the supernatant from centrifuged (9, 000×g, 20min.) leaf homogenate with three fold (by weight) of 0.2M phosphate buffer solution (pH 6.0), avoiding cold acetone soluble parts, being dialyzed against water, and was designated ChIS. To test the inhibitory effect of Chenopodium sap on the infection of non-persistent virus, daikon mosaic virus (DMV) (the Japanese strain of turnip mosaic virus) and its local lesion host, White Burley tobacco were mainly used. Experiments were carried out by abrasion with virus diseased plant sap and also with Chenopodium sap on the half leaves of the lesion host. Inhibitory effect was shown with the percentages obtained by the comparison of the lesion number on treated half leaves with that on the opposite half leaves (controls).1) No decline of inhibitory effect on virus infection of Chenopodium sap heated at 60°C for 10 minutes was observed; while the effect lost when the sap was heated at 100°C for 10 minutes (Table 1, 2, and 3). 2) Inhibitory effect fell remarkably when rubbed with DMV on its original plant, Chenopodium album (Table 4). 3) No inhibitory effect on DMV infection was obtained when DMV was inoculated on upper side of a tobacco leaf soon after its under side was rubbed with ChIS (Table 5). 4) Efficacy of inhibition of ChIS on DMV infection was observed with a 1 to 100 dilution (Fig. 1). Further dilution of the sap resulted remarkable fall of inhibitory effect. 5) Efficacy of inhibition of ChIS on DMV infection was observed even when rubbed 48 hours before the virus inoculation (Table 6). 6) As to after application of ChIS, efficacy of the inhibiting sap on DMV infection was observed up to 30 minutes after the virus inoculation. 7) No inhibitory effect of ChIS on DMV infection was observed when tobacco leaves were syringed or rubbed with ChIS before inoculation of the virus with Myzus persicae (Table 7). 8) No inhibitory effect of ChIS on DMV infection was again observed when tobacco leaves were rubbed with ChIS after inoculation of the virus with M. persicae by brief feeding period of 15 to 20 seconds (Table 8 and 9).To explain the mechanism of the inhibiting action against virus infection of the inhibitor such as Chenopodium sap, the idea that the inhibitor acts on the host cytoplasm and inhibits the formation of virus-receptor complex is now widely accepted.In addition to this a working hypothesis, “Hypersensitive reaction of plant cytoplasm against incompatible inhibitor” is suggested. When such an incompatible inhibitor is introduced and brought in contact with cytoplasm, the latter lose its capability to adsorb virus particles as the results of disorganization due to its hypersensitivity.In the cases of short feeding period of 15 to 20 seconds of M. persicae, the stylet is hardly capable to penetrate through the epidermal layer after it is inserted in between two epidermal cells, and the stylet borne virus as DMV is likely to be transmitted to the plasmodesmata in the intercellular region when stylet tip reaches there. In contrast to this, when DMV is inoculated by abrasion, cuticular layer of the leaf epidermis is scratched off, and the virus is transmitted easily to the disclosed ectodesmata. This histological difference of infectible sites in an epidermal cell-the one plasmodesmata for aphid inoculation, and the other ectodesmata for rubbing inoculations-is the decisive factor why Chenopodium sap is able to inhibit the infection of the virus only when the latter is inoculated by abrasion (Fig. 3).

On the strain distribution of turnip mosaic virus

An attempt was made to distinguish the isolates of turnip mosaic virus into two strains: the one designated the ordinary strain that produces mild symptoms on Brassica oleracea capitata and Nicotiana glutinosa, and the other the cabbage strain that causes severe necrotic ring spot disease on B. oleracea capitata and severe mosaic on N. glutinosa.Turnip mosaic virus isolates which had hitherto been reported by various workers were separated into either of the two strains according to the disease symptoms appearing on the plants mentioned above.An examination was made on geographical distribution of the virus isolates of each of the two strains to see if there was any pattern in the strain distribution.The isolates of the ordinary strain were found in large numbers in India, China, and Japan, but no isolates belonging to the cabbage strain were reported from this area. This led us to assume that the ordinary strain of turnip mosaic virus has its origin in this area.Further, the cabbage strain is indigenous to the area of origin of B. oleracea or its native associates, viz. England or other western Europe.In North America, it was assumed that the two strains were introduced from Europe at about the same time, and that there was also introduction of the ordinary strain from Oriental countries.

STUDIES ON THE METABOLISM OF LEAVES WITH LOCALIZED VIRUS INFECTIONS: I. OXYGEN UPTAKE

Infection of Nicotiana glutinosa with tobacco mosaic virus, of Dianthus barbatus with a carnation virus, of Gomphrena globosa with potato virus X, and of N. tabacum with two strains of turnip mosaic virus produced local lesions and significantly increased O2 uptake to an extent dependent upon the stage of infection. Increased respiration in N. glutinosa, as measured by O2 uptake, was detected 7–10 hours before lesions appeared. When infected plants were maintained at 32 °C, the rise in respiration occurred 8–15 hours before the appearance of lesions, indicating an increase or prolongation of virus multiplication. Local lesion infection of other hosts, though differing in detail, had essentially the same effect. Non-virus injury, including artificially produced necrotic local lesions, did not induce a similar increase in respiration. When necrotic areas were excised from infected disks the remaining portions still respired at a greater rate than healthy controls. Increased respiration appeared to be correlated with virus activity other than the necrotic process.