Details of DPV and References
DPV NO: 362 September 1998
Species: Peach latent mosaic viroid | Acronym: PLMVd
Peach latent mosaic viroid
R. Flores Instituto de Biología Molecular y Celular de Plantas (UPV-CSIC), Universidad Politécnica de Valencia, Camino de Vera 14, 46022, Valencia, Spain
C. Hernández Instituto de Biología Molecular y Celular de Plantas (UPV-CSIC), Universidad Politécnica de Valencia, Camino de Vera 14, 46022, Valencia, Spain
G. Llácer Departamento de Citricultura y Otros Frutales, Instituto Valenciano de Investigaciones Agrarias, 46113 Moncada, Valencia, Spain
J. C. Desvignes Centre Technique Interprofessionel des Fruits et Légumes, Centre de Lanxade, BP 21, F-24130 Prigonrieux, France
- Main Diseases
- Geographical Distribution
- Host Range and Symptomatology
- Transmission by Vectors
- Transmission through Seed
- Transmission by Grafting
- Transmission by Dodder
- Nucleic Acid Hybridization
- Stability in Sap
- Properties of Particles
- Particle Structure
- Particle Composition
- Properties of Infective Nucleic Acid
- Molecular Structure
- Genome Properties
- Relations with Cells and Tissues
- Ecology and Control
Disease first described by
1980). It has many
characteristics in common with those described more than 50 years ago
for the diseases named
(Hutchins et al., 1937;
(Blodgett, 1944) and
North America, and
peach yellow mosaic in Japan
(Kishi et al., 1973),
although a direct comparison is not generally possible because their
inciting agents have never been identified and the typical isolates have
been lost. The viroid nature of the causal infectious agent of peach latent
mosaic was established by
Flores & Llácer (1988) and by
Flores et al. (1990).
A viroid specific to peach and peach hybrids consisting of a circular single-stranded RNA of 336-339 nt. Transmitted by graft propagation, mechanically and to a lesser extent by aphids. Widely distributed around the world.
Infects peach (Prunus persica) usually without inducing obvious leaf symptoms, but very rarely it induces alterations on the peach foliage: yellow-creamy mosaic or white patterns (peach calico), chlorotic mosaic (peach blotch), or small chlorotic leaves with necrotic margins (Fig. 1). The first signs of disorder become apparent 2 years after planting: delay of 4-6 days in foliation, flowering and ripening; irregularly shaped, flattened, colourless fruits with cracked sutures (Fig. 2) and swollen stones; pink broken lines on the rose-white petals in warm temperatures (Fig. 3); bud necrosis; open habit; and rapid ageing of the trees (Fig. 4). Under conditions not well defined, some strains induce furrows in the wood (stem pitting) (Fig. 5).
Recorded in many peach-growing countries particularly in those growing American or Japanese cultivars: USA, Japan, China, and the Mediterranean area: France, Spain, Italy, Greece and Northern Africa (Algeria and Morocco) (Desvignes, 1986; Albanese et al., 1992; Skrzeczkowski, et al., 1996).
Host Range and Symptomatology
The only known host is peach (Prunus persica) and peach
hybrids (almond x peach, plum x peach, etc); other Prunus
species are immune
Recent claims indicate
that it can also infect other Prunus species
(Hadidi et al., 1997;
Faggioli et al., 1997)
but we have not been able to confirm
these results. Transmitted by grafting, budding and experimentally by
Diagnostic and assay species
- Prunus persica (peach) cv. GF-305. Seedlings grown in the
greenhouse are first inoculated by chip budding (10 replicates) with
material from the trees to be analysed, and approximately 2 months later
they are challenge inoculated with a severe isolate (D168). Plants
previously infected with a latent strain of PLMVd do not display the
characteristic chlorotic mosaic of the severe isolate. This selected severe
strain is not totally stable (some plants revert to a symptomless condition)
and is maintained in the greenhouse by re-inoculating it monthly. This
cross-protection assay between the two types of PLMVd strains
has allowed the study and control of the disease in
PLMVd can also be detected by molecular methods including polyacrylamide gel electrophoresis (Flores & Llácer, 1988; Flores et al., 1990), dot-blot hybridization with radioactive and non- radioactive probes (Ambrós et al., 1995; Loreti et al., 1995), and RT-PCR (Shamloul et al., 1995) with primers derived from the reference sequence (Hernández & Flores, 1992). By molecular hybridization, Ambrós et al. (1995) have shown the presence of PLMVd in several Japanese peach cultivars displaying the characteristic symptoms of peach yellow mosaic disease, suggesting that it is the cause of this disease. However, by RT-PCR Shamloul et al. (1995) have been unable to detect PLMVd in some American isolates of peach mosaic so that peach latent mosaic and peach mosaic should be considered as two distinct diseases incited by a viroid and another pathogen, presumably a virus, respectively.
- Prunus persica is the only host from which the viroid has been purified.
Most isolates do not incite symptoms on peach seedlings in the greenhouse. However, some isolates (D168) induce a general chlorotic mosaic, sometimes necrotic, or rarely a yellow mosaic, and others stem pitting (Desvignes, 1980). Minor differences in nucleotide sequence have been observed between two different complementary DNA clones from a French isolate (Hernández & Flores, 1992) and with respect to an Italian isolate (Shamloul et al., 1995).
Transmission by Vectors
PLMVd is transmitted by aphids (Myzus persicae) (Desvignes, 1981; Flores et al., 1992) but not by pollen or mites (Desvignes, 1981).
Transmission through Seed
No seed transmission reported (Desvignes, 1986; Flores et al., 1992).
PLMVd exhibits very limited sequence similarities with other viroid and viroid-like satellite RNAs and does not have any of the central conserved regions characteristic of most typical viroids. However, PLMVd has the elements required to form in the RNAs of both polarities the hammerhead structures proposed to act in the in vitro self-cleavage of avocado sunblotch viroid (ASBVd) (Hutchins et al., 1986), chrysanthemum chlorotic mottle viroid (CChMVd) (Navarro & Flores, 1997) and some satellite RNAs (Bruening, 1989; Symons, 1989). Plus and minus RNA transcripts of PLMVd containing the hammerhead structures display self-cleavage during transcription and after purification. These results support the inclusion of PLMVd in a viroid family represented by ASBVd, whose members are characterized by their ability to self-cleave in vitro and very probably in vivo through hammerhead structures (Hernández & Flores, 1992).
Stability in Sap
The viroid can be purified from infected leaves or young fruits of peach (Flores & Llácer 1988; Flores et al., 1990). The tissue is extracted with buffer-saturated phenol, and the nucleic acids are partially purified by chromatography on non-ionic cellulose (CF-11). Polysaccharides can be removed by treatment with 2-methoxyethanol and subsequent recovery of the nucleic acids by precipitation with cetyltrimethylammonium bromide. Viroid circular molecules are obtained by two consecutive steps of polyacrylamide gel electrophoresis under non-denaturing and denaturing conditions, and final elution from the gel.
Properties of Infective Nucleic Acid
A covalently closed single-stranded RNA. The sequence of the reference variant of 337 residues has a base composition (G:A:C:U) of 27.0 : 23.7 : 25.5 : 23.7 which adopts a branched conformation (Fig. 6) in the proposed secondary structure of minimum free energy (Hernández & Flores, 1992).
Relations with Cells and Tissues
The viroid can be isolated from leaves, fruits, stems and roots of infected peach plants (Flores et al., 1992), both from those that are symptomlessly infected and from those displaying typical disease symptoms.
Ecology and Control
The main control measure is the use of viroid-free planting material. The agent can be eliminated from infected peach trees, although with some difficulty, by growing plants in hot air at 37 °C for 35-45 days, followed by propagation of the tips (Desvignes, 1986).
Variability of the foliar symptoms induced by PLMVd (severe strain D168) on GF-305 peach seedlings. From left to right: leaves 1-3 showing blotching and mosaic, leaf 4 chlorotic creamy calico, leaf 5 chlorosis with necrotic margins.
Primary and proposed secondary structure of lowest free energy for the reference sequence variant of PLMVd (M83545). Plus and minus self-cleavage domains are delimited by flags, the 13 conserved residues present in most of the hammerhead structures are indicated by bars, and the self-cleavage sites are shown by arrows. Solid and open symbols refer to plus and minus polarities respectively (adapted with modifications from Hernández & Flores, 1992).
References list for DPV: Peach latent mosaic viroid (362)
- Albanese, Giunchedi, La Rosa, & Poggi-Pollini, Acta Hort. 309: 331, 1992.
- Ambrós, Desvignes, Llácer & Flores, Acta Hort. 386: 515, 1995.
- Blodgett, Phytopathology 34: 650, 1944.
- Bruening, Methods Enzymol. 180: 546, 1989.
- Desvignes, Acta Hort. 67: 315, 1976.
- Desvignes, Acta phytopath. Acad. Sci. hung. 15: 183, 1980.
- Desvignes, 1er Colloque Rech. Fruitières - Bordeaux, 263, 1981.
- Desvignes, Acta Hort. 130: 89, 1982.
- Desvignes, Acta Hort. 193: 51, 1986.
- Faggioli, Loreti, & Barba, Pl. Dis. 81: 423, 1997.
- Flores, & Llácer, Acta Hort. 235: 325, 1988.
- Flores, Hernández, Desvignes, & Llácer, Res. Virol. 141: 109, 1990.
- Flores, Hernández, Avinent, Hermoso, Llácer, Juárez, Arregui, Navarro, & Desvignes, Acta Hort. 309: 325, 1992.
- Hadidi, Giunchedi, Shamloul, Poggi-Pollini, & Amer, Pl. Dis. 81: 154, 1997.
- Hernández, & Flores, Proc. natn. Acad. Sci. U.S.A. 89: 3711, 1992.
- Hutchins, Bodine, & Thornberry, Circ. U.S. Dept. Agric. 427, 1937.
- Hutchins, Rathjen, Forster, & Symons, Nucleic Acids Res. 14: 3627, 1986.
- Kishi, Takanashi, & Abiko, Bull. hort. Res. Stn. A. 12: 197, 1973.
- Loreti, Faggioli, & Barba, Acta Hort. 386: 560, 1995.
- Navarro, & Flores, Proc. natn. Acad. Sci. U.S.A. 94: 11262, 1997.
- Stout, Bull. Dept. Agric. Calif. 28: 117, 1939.
- Shamloul, Minafra, Hadidi, Giunchedi, Waterworth, & Allam, Acta Hort. 386: 522, 1995.
- Skrzeczkowski, Howell, & Mink, Pl. Dis. 80: 823, 1996.
- Symons, Trends Biochem. Sci. 14: 445, 1989.
- Willison, Phytopathology 36: 273, 1946.