This article was downloaded by: [Washburn University]On: 31 October 2014, At: 23:41Publisher: Taylor & FrancisInforma Ltd Registered in England and Wales Registered Number: 1072954Registered office: Mortimer House, 37-41 Mortimer Street, London W1T3JH, UK

New Zealand Journal ofAgricultural ResearchPublication details, including instructions forauthors and subscription information:http://www.tandfonline.com/loi/tnza20

Occurrence of cherry greenring mottle virus in NewZealandE.E. Chamberlain a , J.D. Atkinson a , G. A. Wood b

& J. A. Hunter ba Plant Diseases Division, Department of Scientificand Industrial Research , Private Bag, Auckland ,New Zealandb Warwick Farm. R.D.I , Morrinsville , New ZealandPublished online: 24 Jan 2012.

To cite this article: E.E. Chamberlain , J.D. Atkinson , G. A. Wood & J.A. Hunter (1971) Occurrence of cherry green ring mottle virus in NewZealand, New Zealand Journal of Agricultural Research, 14:2, 499-508, DOI:10.1080/00288233.1971.10427112

To link to this article: http://dx.doi.org/10.1080/00288233.1971.10427112

PLEASE SCROLL DOWN FOR ARTICLE

Taylor & Francis makes every effort to ensure the accuracy of allthe information (the “Content”) contained in the publications on ourplatform. However, Taylor & Francis, our agents, and our licensorsmake no representations or warranties whatsoever as to the accuracy,completeness, or suitability for any purpose of the Content. Any opinionsand views expressed in this publication are the opinions and views ofthe authors, and are not the views of or endorsed by Taylor & Francis.The accuracy of the Content should not be relied upon and should beindependently verified with primary sources of information. Taylor andFrancis shall not be liable for any losses, actions, claims, proceedings,demands, costs, expenses, damages, and other liabilities whatsoeveror howsoever caused arising directly or indirectly in connection with, inrelation to or arising out of the use of the Content.

This article may be used for research, teaching, and private studypurposes. Any substantial or systematic reproduction, redistribution,reselling, loan, sub-licensing, systematic supply, or distribution in any form

to anyone is expressly forbidden. Terms & Conditions of access and use canbe found at http://www.tandfonline.com/page/terms-and-conditions

Dow

nloa

ded

by [

Was

hbur

n U

nive

rsity

] at

23:

41 3

1 O

ctob

er 2

014

499

OCCURRENCE OF CHERRY GREEN RING MOTTLE VIRUS IN NEW ZEALAND

By E. E. CHAMBERLAIN*. J. D. ATKINSON*. G. A. WOOD*. AND J. A. HUNTER t

(Received 13 October 1970)

ABSTRACT

A disease of flowering cherry characterised by epinasty of foliagc, stunting of trees, and roughening of bark, and accompanied by excessive graft failures, caused serious losses in two nurseries on Kanzan and three other varieties. The causal agent was diagnosed as cherry grccn ring mottle virus (GRMV). Infection was shown to come from mazzard rootstocks raised from root cuttings taken from sweet cherry nursery trees. Complete control in the nurseries was achieved by the use of mazzard seedling rootstocks. The virus, carried without symptoms, was found to be prevalent in sweet and mazzard cherries and to occur in some peach and nectarine varieties.

INTRODUCTION

The virus disease cherry green ring mottle (GRMV) was first recognised during the 1930's in North America. where it is regarded primarily as a disease of sour cherry (Prunus cerasus L.) (Rasmussen et al. 1951). The disease described by Milbrath and Zeller (1942) on Kanzan (syn. Kwanzan) as 'Rough bark. a virus disease of flowering cherry' would appear to have been caused by the same virus.

In New Zealand, during January 1957. specimens of grafted nursery trees of Kanzan flowering cherry (P. serrulata Lind!.) showing stunted growth, epinasty of foliage. and roughening of bark were received from a South Island nursery where this condition, coupled with failure of grafts. was causing serious losses. The symptoms on these specimens closely resembled those of the rough bark disease described by Milbrath and Zeller (1942). However. the roughening of bark was not a con­sistent feature of the disease. epinasty of foliage being the most charac­teristic symptom. In New Zealand the disease was recorded as 'Epinasty of Oriental flowering cherry' (Chamberlain 1961) and later as 'Cherry (flowering) rough bark virus' (Dingley 1969).

Milbrath and Zeller (1945) found that when buds of sweet cherry (P. avium L.) were inserted in Kanzan trees the latter frequently devel­oped epinasty of foliage, which has since been shown by Fridlund and

• Plant Diseases Division, Department of Scientific and Industrial Research, Private Bag, Auckland, New Zealand.

t Retired: Warwick Farm. R.D.I, Morrinsville. New Zealand.

N.Z. lournal of Agricultural Research (1971), 14: 499-508

Dow

nloa

ded

by [

Was

hbur

n U

nive

rsity

] at

23:

41 3

1 O

ctob

er 2

014

500 Cherry green ring mottle virus

Diener (1958) to be caused by GRMV. The latter authors also showed that GRMV was a distinct virus not related to sour cherry yellows virus, of which it had been regarded as a strain (Rasmussen et al. 1951). These findings were confirmed by Barksdale (1959) and Milbrath (1960). The latter showed that in the absence of Prunus necrotic ring spot virus, GRMV could cause an epinasty reaction in Shirofugen flow­ering cherry, and also suggested that this virus might have been the cause of the rough bark condition on Kanzan described by Milbrath and Zeller (1942).

SYMPTOMS

Montmorency sour cherry

The name GRMV was given to the virus because in North America on Montmorency sour cherry it produces green spots, rings, arcs, or irregular curved bands on yellowed leaves (Rasmussen et al. 1951). It also causes pitting of fruit (Parker and Klos 1953; Barksdale 1959). Montmorency is not grown commercially in New Zealand, and no symptoms have developed on leaves of experimentally infected trees. Failure of symptoms to develop at this laboratory is probably the result of climatic differences between here and North America.

Flowering cherry

On infected plants of Kanzan flowering cherry in New Zealand the most characteristic symptom is epinasty of leaves, which curl down­wards at the tips, are distorted, smaller than normal, have chlorotic areas associated with the veins, and necrotic lesions on midribs and secondary veins (Figs 1 and 2). Also, infected trees may be stunted and the bark roughened (Figs 3 and 4). Symptoms range in severity from mild to severe:

Mild: Leaves almost normal in size but distorted and curled; growth slightly stunted with slightly shortened internodes but no die­back; bark normal.

Moderate: Leaves smaller than normal, distorted and curled; growth considerably stunted with shortened internodes but no dieback; bark brown and slightly roughened (Fig. 3).

Although trees with moderate symptoms continue to grow, their growth is considerably retarded (Fig. 5), and leaf epinasty and bark roughening persist.

Severe: Leaves much distorted and curled with a tendency to fall prematurely to leave partially bare stems (Fig. 1); growth much stunted with considerably shortened internodes and dieback of some shoots; bark brown and severely roughened and cracked (Fig. 4).

These symptoms correspond closely to those described on Kanzan by Milbrath and Zeller (1942; 1945) and Milbrath (1952; 1960).

On the varieties Ko Fugen, Shirotae (Mount Fuji), and Takasago (Sieboldii), under local conditions, foliage symptoms and stunting of

Dow

nloa

ded

by [

Was

hbur

n U

nive

rsity

] at

23:

41 3

1 O

ctob

er 2

014

E. E. CHAMBERLAIN et al. 501

Fig: I (left) -Com­panson of shoots from healthy (left) and GRMV-infected (right) Kanzan flow­ering cherry. Infected shoot shows distorted leaves curled down­wards at tips and pre-

mature leaf fall. [Photo S. A. Rumsey

Fig. 2 (below)­Leaves of GRMV­infected Kanzan flow­ering cherry showing distortion, curling, chlorotic areas along veins, 'lnd necrotic lesions on underside of mid-rib and secon-

dary veins. X It [Photo S. A. Rumsey

Dow

nloa

ded

by [

Was

hbur

n U

nive

rsity

] at

23:

41 3

1 O

ctob

er 2

014

502 Cherry green ring mottle virus

Fig. 3-Roughening of bark on branch (left) of Kanzan flowering cherry infected with a moderate strain of GRMV. Branch on right from

healthy tree. X t [Photo 1. W. Endt

Fig. 4- -Roughening and splitting of bark on branch (right) of Kanzan flowering cherry infected with a severe strain of GRMV. Branch from

healthy tree on left. X ! [Photo 1. W. Endt

growth appear to be less pronounced, and roughening of bark has not been observed.

Other Prunus species

In New Zealand, 'as in North America (Barksdale 1959; Fridlund 1961), GRMV does not produce symptoms on sweet cherry, mazzard cherry, peach (P . persica (L.) Batsch), or nectarine (P. persica var. nucipersica (Borkh.) C. K. Schneider).

INCIDENCE

GRMV is widespread in stone fruit species in North America. Incidence is high in sweet cherry (Gilmer 1961; Fridlund 1963), in sour cherry in some orchards (Barksdale 1959), and in some peach varieties (Cation 1967). It also occurs in apricot (P . armeniaca L.), duke cherry (P. avium X P. cerasus), mazzard cherry, and nectarine (Fridlund

Dow

nloa

ded

by [

Was

hbur

n U

nive

rsity

] at

23:

41 3

1 O

ctob

er 2

014

E. E. CHAMBERLAIN et al.

Fig. 5---Comparison of IO-year-old healthy (left) and GRMV­infected (right) Kanzan flowering cherry trees. Stunting caused by a

moderate strain of the virus. [Photo A. Underhill

503

1961). In flowering cherry Milbrath and Zeller (1942) reported an incidence of over 15 percent in a planting of 3,887 Kanzan nursery trees in an Oregon nursery. The virus also occurs in Canada (Rasmussen et al. 1951). but, although its presence has been demonstrated on the sweet cherry variety Bing in Switzerland (Schmid 1963), little is known regarding its incidence in countries outside North America.

Flowering cherry

In the New Zealand nursery where GRMV infection of flowering cherry was first found losses were greatest in the popular Kanzan variety, but Takasago was also affected. Inspection of other nurseries raising flowering cherry trees revealed that a similar problem occurred in another smaller nursery.

During the following season a survey was made of the Kanzan trees growing in the larger nursery. Of the 1,893 trees originally grafted,

Dow

nloa

ded

by [

Was

hbur

n U

nive

rsity

] at

23:

41 3

1 O

ctob

er 2

014

504 Cherry green ring mottle virus

only 909 appeared to be healthy. The remaining 984 were represented by 105 trees showing mild epinasty symptoms of GRMV and 879 gaps which had been left after nursery staff had removed weak trees, those showing severe epinasty, and stocks on which grafts had failed. Because so many trees had been removed it was not possible to determine the actual number of trees that had been infected, but it was obviously much greater than the 105 recorded during the survey. Although no detailed survey was made of other flowering cherry varieties, epinasty was observed on Ko Fugen and Shirotae.

Since GRMV was discovered on flowering cherry a number of trees of common stone fruit species have been indexed on Kanzan to determine whether they carry the virus.

Sweet and mazzard cherries

The sweet cherry trees indexed were vigorous, apparently healthy trees of varieties that had been established in New Zealand for many years. The mazzard trees, retained in sweet cherry orchards as pollin­ators, had originated from stocks on which sweet cherry scions had failed, so it is likely that any infection would have come from the sweet cherry scions.

Of a total of 18 trees, including 10 sweet cherry varieties, that were indexed, all except 2 were infected. The virus was present in all trees of Bedford Prolific, Bigarreau Pelissier. Chapman, Dawson (Noir de Guben), Early Cluster, Early Lyons, Werder's Early Black, and William's Favourite. One tree of Florence and one of St. Margaret were not infected.

Four of the 6 mazzard cherry trees included in the trials were infected.

Peach and nectarine

Single trees of 21. peach and 7 nectarine varieties were indexed. The peach varieties included some that had been grown here since the beginning of the century and others more recently introduced from North America and South Africa. Infection was found only in the North American variety Halehaven. Although grown in New Zealand for over 20 years, it was probably infected when introduced, for Cation (1967) concluded that the original Halehaven tree had acquired the virus before the first budwood was distributed.

The nectarine varieties included one selected in New Zealand and 6 introduced from North America during the past 10 years. Infection was found only in the North American varieties Le Grand and New Yorker.

Apricot, almond, and Japanese plum

Indexing of single trees of 5 long-established apricot varieties and 2 trees each of the New Zealand selected almond Monavale and the Japanese plum variety Billington showed that all were free from GRMV.

Dow

nloa

ded

by [

Was

hbur

n U

nive

rsity

] at

23:

41 3

1 O

ctob

er 2

014

E. E. CHAMBERLAIN et al. 505

METHODS OF SPREAD

Field surveys in North America indicate that natural spread of GRMV occurs in sour cherry orchards (Parker and Klos 1953; Barks­dale 1959). The actual means of spread is not known, but Kable and Parker (1968), from studies of rate and pattern of orchard spread, concluded that it was unlikely that the virus was pollen transmitted or carried from tree to tree by nematodes or leaf hoppers. They showed that the virus was able to infect the milkweed Asclepias syriaca and, in an orchard survey, found an apparent relationship between GRMV incidence and milkweed populations. They suggested that the milkweed might act as an alternative host from which the virus was spread to sour cherry by some unknown vector.

Spread in North America occurs also through propagation. Mil­brath and Zeller (1942) found that the presence of the virus in flowering cherry nursery trees resulted from the use of scionwood from infected parent trees. Fridlund (1963) considered that high incidence of GRMV in sweet cherry in western U.S.A. did not necessarily indicate consider­able natural field spread, as circumstantial evidence suggested that nursery and orchard practices could be responsible. In particular the practice of top working trees of modem commercial varieties with scions from older varieties to act as pollinators could have done much to spread infection.

The virus appears not to be transmitted in the seed of sweet, sour, or mazzard cherry or peach (Gilmer and Brase 1962; Fridlund 1966; Cation 1967).

No information is available on natural spread under New Zealand conditions, but the virus is known to be spread by nursery practices. When the disease was investigated at the nursery where it was first discovered, the parent Kanzan trees used as a source of scionwood were found to be free from infection. It appeared, therefore, that infec­tion must have come from the rootstocks.

Normally rootstocks were raised from root cuttings taken from mazzard cherry stocks, originally raised from seed, as they were lifted from the stock bed for lining out. However, the number of available cuttings was not always sufficient for the formation of a new stock bed, so additional root cuttings were obtained from grafted trees of sweet and flowering cherries as they were being lifted for sale. Since GRMV is carried in a high proportion of our sweet cherry trees, many of the grafted nursery trees would have become infected, and root cuttings from them would have intrcxluced infection into the stock bed. Presence of the virus in the rootstocks was verified by indexing with Kanzan. Of 21 stocks indexed, scions failed on 2, and one of the remaining Kanzan scions developed epinasty symptoms typical of GRMV in­fection. Since the rootstocks were used to raise both flowering and sweet cherry trees, any virus in the stocks would have passed into the scions of both species.

It is probable that the virus was introduced into the other affected nursery in the same way, for there, too, rootstocks were raised from root cuttings.

Dow

nloa

ded

by [

Was

hbur

n U

nive

rsity

] at

23:

41 3

1 O

ctob

er 2

014

506 Cherry green ring mottle virus

ECONOMIC IMPORTANCE

In North America GRMV is of considerable economic importance because it is widespread in Montmorency sour cherry and reduces quality of fruit or renders it unmarketable through pitting and poor flavour (Parker and Klos 1953; Barksdale 1959). On flowering cherry it has been of limited importance, having been reported in one nursery only (Milbrath and Zeller 1942).

In New Zealand it caused substantial losses of flowering cherry nursery trees in two nurseries before control measures were introduced.

On other hosts GRMV does not appear to have any appreciable effect. It is carried without symptoms and appears not to interact syn­ergistically with other common stone fruit viruses to cause disease in­tensification (Barksdale 1959; Pine 1964). Pine (1964) showed that it had little or no effect on yield of peach.

CONTROL MEASURES

When it was discovered that· G RMV infection was coming from rootstocks the nurserymen concerned were advised to use mazzard seedlings instead of stocks raised from root cuttings. The change-over took several years, but by 1966 approximately half the flowering cherries in the larger nursery were being grown on seedlings. A comparison of Kanzan trees on the two types of rootstocks gave a measure of the control achieved. Of 100 trees grafted on seedlings, 94 were vigorous and healthy, grafts having failed on the remaining 6. Of 100 trees on rootstocks raised from root cuttings, 44 were vigorous and healthy, 5 showed symptoms of GRMV, and grafts had failed on 51. By 1968 all flowering cherries were being grown on seedling rootstocks, and no symptoms of GRMV could be found in any of the varieties including Kanzan. Growth was vigorous and uniform in all varieties and the number of graft failures was low throughout.

To improve the disease status of all stone fruit species grown in New Zealand an effort is being made by selection and/or heat treatment to obtain trees free from known viruses, including GRMV.

It has been shown elsewhere that GRMV is able to survive heat treatment which eliminates Prunus necrotic ring spot virus (Milbrath 1960), and preliminary trials here confirm that it is resistant to heat therapy. However, we have some evidence that it is possible to eliminate the virus by heat treatment followed by trip propagation. One Bigarreau Pelissier sweet cherry tree raised from a shoot tip taken from a GRMV­infected tree grown at 100°F for 28 days and grafted to a mazzard cherry seedling was found to be free from this virus. Further heat treatment trials are in progress.

DISCUSSION

Barksdale (1959) found that GRMV was the only virus common on sour cherry in New York State to cause epinasty on Kanzan, and since

Dow

nloa

ded

by [

Was

hbur

n U

nive

rsity

] at

23:

41 3

1 O

ctob

er 2

014

E. E. CHAMBERLAIN et al. 507

no other stone fruit virus has been reported to produce such symptoms on flowering cherry, it seems that epinasty is diagnostic of GRMV only. As the epinasty symptoms occurring here on flowering cherry closely correspond to those described in North America, it is concluded that the New Zealand disease is caused by GRMV. Also, there would appear to be little doubt that the 'rough bark of flowering cherry' des­cribed by Milbrath and Zeller (1942) was caused by the same virus. Milbrath (1960) reported that GRMV was present in the source tree from which the rough bark disease had originated, and suggested that it might have been caused by a specific strain of the virus. Later he (Milbrath 1966) produced evidence to show that GRMV occurred in a number of strains, causing mild to severe symptoms. There seems to be no reason why the virus, which caused rough bark of flowering cherry, should not be regarded as a severe strain of GRMV and the name 'cherry (flowering) rough bark virus' classed as a synonym.

There is some evidence that GRMV causes incompatability between stock and scion. When Milbrath and Zeller ( 1942) inserted healthy Kanzan buds in mazzard seedling rootstocks, 88 percent of the scions grew, but when they used GRMV infected buds, only 24 percent sur­vived. Many of the graft failures in the New Zealand nurseries were probably caused by GRMV infection, although other viruses could have been involved. It is now known that Prunus necrotic ring spot and prune dwarf viruses are prevalent in our sweet cherries (Fry and Wood 1971), and these viruses would have entered the mazzard rootstocks along with GRMV.

The fact that the nursery where GRMV was first recognised suffered over 50 percent loss of nursery trees through virus contamination of rootstocks emphasises the danger of obtaining propagating material from worked trees.

Acknowledgments

The authors acknowledge assistance by officers of the Horticulture Division, Department of Agriculture, and in particular that of Messrs A. T. J. Watts, C. S. Richardson, and J. D. Galletly, who carried out the nursery surveys. We also acknowledge the co-operation and assistance of the nurserymen involved.

REFERENCES

BARKSDALE, T. H. 1959: Phytopathology 49: 777-84.

CATION, D. 1967: Plant Disease Reporter 51: 261-3.

CHAMBERLAIN, E. E. 1961: Orchardist of N.Z. Supplement (10), 34. 8 pp.

DINGLEY, J. M. 1969: N.Z. Department of Scientific and Industrial Research Bulletin 192. 298 pp.

FRIDLUND, P.R. 1961: Plant Disease Reporter 45: 687-9.

----- 1963: Ibid 47:345-7.

----- 1966: Ibid. 50: 902-4.

-----;DIENER, T. 0. 1958: Ibid. 42:830-2.

Dow

nloa

ded

by [

Was

hbur

n U

nive

rsity

] at

23:

41 3

1 O

ctob

er 2

014

508 Cherry green ring mottle virus

FRY, P. R.; WOOD, G. A. 1971: N.Z. Journal of Agricultural Research 14: 515-25.

GILMER, R. M. 1961: Plant Disease Reporter 45: 612-5.

----~; BRASE, K. D. 1962: Ibid. 46: 356.

KABLE, P. F.; PARKER, K. G. 1968: Phytopathology 58: 1443--4.

MILBRATH, J. A. 1952: Oregon State College Agricultural Experiment Station Bulletin 522. 27 pp.

----~-- 1960: Phytopathology 50: 495-7.

1966: Plant Disease Reporter 50: 59-62.

-----~; ZELLER, S. M. 1942: Phytopathology 32: 428-30.

1945: Science, N.S. 101: 114-5.

PARKER, K. G.; Kws, E. J. 1953: Abs. in Phytopathology 43: 481.

PINE, T. S. 1964: Phytopathology 54: 604-5.

RASMUSSEN, E. J.; BERKELEY, G. H.; CATION, D.; HILDEBRAND, E. M.; KEITT, G. W.; MOORE, J. D. 1951: In "Virus Diseases and Other Disorders with Viruslike Symptoms of Stone Fruits in North America". U.S. Department ot Agriculture Handbook 10: 159-61.

SCHMID, G. 1963: Schweiz. Z. Obst u. Weinb. 72: 55-60.

Dow

nloa

ded

by [

Was

hbur

n U

nive

rsity

] at

23:

41 3

1 O

ctob

er 2

014