Natural Spread, Graft-transmission, and Possible Etiology of Walnut Blackline Disease

Mircetich, S. M.; Sanborn, R; Ramos, D. E.

doi:10.1094/phyto-70-962

Cited by 45 publications

(20 citation statements)

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“…Most former cases of "delayed" incompatibility have now been identified as diseases, such as pear decline by mycoplasma-like organisms (Hibino et al 1971), walnut blackline disease caused by cherry leafroll virus (Mircetich et al 1980), prune brownline disease caused by a strain oftomato ringspot virus, Tom RSVP (Mircetich and Hoy 1981), apple union necrosis and decline caused by tomato ringspot virus (Cummins and Gonsalves 1982), and the X-disease aberration of cherry (Uyemoto 1989). The time involved in transfer of the pathogen and expression of the disease symptoms, as well as possible production of toxic metabolites during senescence, delays graft failure.…”

Section: Typesmentioning

confidence: 99%

Graft Incompatibility

Andrews¹,

Márquez²

1993

Horticultural Reviews

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Section: Typesmentioning

confidence: 99%

Graft Incompatibility

Andrews¹,

Márquez²

1993

Horticultural Reviews

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“…Its genome is composed of two positivesense polyadenylated ssRNAs which carry a genomelinked protein (VPg) at their 5' ends (Hellen & Cooper, 1987). The walnut strain of CLRV (wCLRV) is consistently associated with the causal agent of the lethal disease of graft incompatibility in walnuts known as blackline (Mircetich et al, 1980). This paper deals with the pattern of accumulation of CLRV in a systemic infection of tobacco plants and the influence of leaf ontogeny and the phyllotactic position of the leaves on susceptibility to virus infection.…”

Section: Introductionmentioning

confidence: 99%

Long-distance movement of cherry leaf roll virus in infected tobacco plants

Más

Pallás

1996

Journal of General Virology

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The long-distance movement of cherry leaf roll virus (CLRV) in tobacco plants was studied using a tissue printing technique with non-isotopic RNA probes. Time-course analysis revealed that CLRV RNA accumulated in the inoculated leaf at an early stage, such as 20 h post-inoculation. The virus accumulation reached a peak at 8-10 days post-inoculation (d.p.i.) and then progressively decreased. The virus RNA signal was detected before the appearance of symptoms. The virus invaded stem vascular tissues at 3 d.p.i., moving towards the roots before moving to the upper leaves. In systemically infected leaves, the virus appeared first in the basal regions and then moved to the distal parts through the vascular system. The distribution pattern of the virus coat protein in systemically infected leaves was parallel to that observed for the virus RNA, suggesting that CLRV requires the coat protein for long-distance movement. The movement of the virus was influenced by the phyllotactie position of the leaves. The viral symptoms and the virus RNA signal in older systemically infected leaves were asymmetrically distributed, being localized in the side of the lamina closest to the inoculated leaf. Virus distribution in infected plants as well as the susceptibility of the plant to systemic infection were also influenced by the developmental stage of the inoculated leaves. Inoculation of leaves at 95 % of their final size resulted in virus replication but no systemic infection. In fully mature leaves the virus did not replicate.

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“…However, in many hosts, unrestricted seed-and pollenmediated spread occurs, resulting in significant CLRV prevalence in forests and other natural environments (Rebenstorf et al, 2006;Jalkanen, 2007) or in some cultivated crops (Mircetich et al, 1980). grapevine, Prunus spp., Rubus spp., olive), the existence of efficient and widely adopted voluntary certification systems constitutes a strong limitation to the spread of CLRV through the plants for planting pathway.…”

Section: Spread Capacitymentioning

confidence: 99%

“…This includes decline in American elm (Mayhew and Epstein, 1971); tree decline or death in cherry, in particular in situations of co-infection with Prunus necrotic ringspot virus and Prune dwarf virus (Cropley, 1961;Jones, 1985;Büttner, 2011); and decline and death of European walnut (Juglans regia) scions grafted onto Northern California black walnut (J. hindsii), "Paradox" hybrids (J. hindsii × J. regia), Chinese wingnut (Pterocarya stenoptera) or other sensitive Juglans spp. Although CLRV remains symptomless or causes only foliar symptoms in many cultivars of J. regia, it causes tissue necrosis (resulting in a black or brown line of necrotic tissues) at the scion-rootstock junction of susceptible graft combinations, eventually girdling and killing the tree (Mircetich et al, 1980;Rowhani and Mircetich, 1988). Although CLRV remains symptomless or causes only foliar symptoms in many cultivars of J. regia, it causes tissue necrosis (resulting in a black or brown line of necrotic tissues) at the scion-rootstock junction of susceptible graft combinations, eventually girdling and killing the tree (Mircetich et al, 1980;Rowhani and Mircetich, 1988).…”

Section: Potential Effects Of Cherry Leafroll Virusmentioning

confidence: 99%

Scientific Opinion on the pest categorisation ofCherry leafroll virus

Rossi¹

2014

EFSA Journal

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The Panel on Plant Health performed a pest categorisation of Cherry leafroll virus (CLRV) for the European Union (EU) territory. CLRV is a well-defined virus species of the genus Nepovirus, for which the entire genome sequence and molecular detection assays are available. CLRV is transmitted by vegetative multiplication of infected hosts and is also seed-and pollen-transmitted (both horizontally and vertically) in many of its hosts. There is, however, evidence that interspecific transmission by the pollen-mediated mechanism is very limited. CLRV has a wide host range, which contains both woody and herbaceous hosts, many of which are largely present in natural environments. It is listed on plants of Rubus spp. for planting in Annex IIAI of Directive 2000/29/EC. CLRV is widely present in the EU but there are very few records on its regulated hosts. It is not expected to be affected by ecoclimatic conditions wherever its hosts are present and has the potential to establish in large parts of the EU territory. CLRV can spread through efficient seed-and pollen-mediated transmission mechanisms and through the movement of vegetatively propagated plants for planting of numerous hosts. However, the existence of efficient and widely adopted certification systems for some of these hosts constitutes a limitation to CLRV spread. Although the virus alone or when in mixed infection can cause significant disease in some hosts, the actual impact of CLRV is very difficult to evaluate but generally appears to be limited.

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Natural Spread, Graft-transmission, and Possible Etiology of Walnut Blackline Disease

Cited by 45 publications

References 0 publications

Graft Incompatibility

Graft Incompatibility

Long-distance movement of cherry leaf roll virus in infected tobacco plants

Scientific Opinion on the pest categorisation ofCherry leafroll virus

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