Plant Breeding 126, 449—453 (2007) 2007 The Authors
Journal compilation  2007 Blackwell Verlag, Berlin

doi:10.1111/j.1439-0523.2007.01379.x

Resistance sources to Valsa canker (Valsa ceratosperma) in a germplasm collectionof diverse Malus species
K . A b e 1 , N . K o t o d a 1 , H . K a t o 1 and J . S o e j i m a 2
1
Apple Research Station, National Institute of Fruit Tree Science, Morioka, Iwate 020-0123, Japan, E-mail: kazuyuki@
aﬀrc.go.jp; 2National Institute of Fruit Tree Science, Tsukuba, Ibaragi 305-8605, Japan

With 1 table
Received August 30, 2006/Accepted January 16, 2007
Communicated by W. E. Weber

Abstract
Although Valsa canker caused by Valsa ceratosperma (Tode ex Fr.)
Maire is one of the most destructive diseases in apple (Malus · domestica Borkh.) especially in eastern Asia, information available to help
with breeding against Valsa canker in apples is limited. In this work, 53
accessions of diverse Malus species and their interspeciﬁc hybrids were
tested for resistance to V. ceratosperma, using an excised shoot assay.
Dormant shoots and succulent growing shoots from each accession
were inoculated with a virulent isolate AVC-12 of V. ceratosperma,
and the length of necrosis was measured at 10 days post-inoculation
for the dormant shoots and at 7 days post-inoculation for the growing
shoots. The lesion length relative to the susceptible control ÔFuji’ indormant shoots (RLD) and to that in growing shoots (RLG) were
simple but useful parameters to diﬀerentiate between resistant andsusceptible accessions. Fourteen accessions from M. baccata,
M. ﬂorentina, M. halliana, M. micromalus, M. pratii, M. sieboldii,
M. yunnanensis, M. · ﬂoribunda and M. · platycarpa gave low RLD
and RLG values of less than 0.6 and were evaluated as resistantregardless of the diﬀerence in the stage of growth. The highest level ofresistance was found in M. sieboldii. This high level of resistance in
M. sieboldii was eﬀective against diﬀerent isolates of V. ceratosperma.

Key words: Malus species — Valsa ceratosperma — artiﬁcial
inoculation
Valsa canker, caused by Valsa ceratosperma (Tode ex Fr.)
Maire (syn. Valsa mali Miyabe et Yamada), is one of the mostimportant diseases of apple; the disease has seriously limited
apple production, especially in eastern Asia (Sakuma 1990,
Sawamura et al. 1990, Uhm and Sohn 1995). The causal
fungus infects the trees through wounds such as the pruning
ends or fruit scars. Most new lesions, infected trunks, shootand fruit scars, appear in spring, and the canker develops
rapidly between spring and early summer, and then slowly
during the rest of the summer and in the winter. Infection
produces localized cankers, and then brings about the death oftwigs, limbs or the entire tree afterwards. As the mycelium of
the causal fungus is able to invade healthy tissues of bark,phloem and xylem extensively (Tamura and Saito 1982) andbecause of the perennial nature of the canker, as with stem
canker of apple caused by Botryosphaeria dothidea andB. obtusa (Brown-Rytlewski and McManus 2000), spray
applications of fungicides are not always successful for thecontrol of Valsa canker.
Genetic resistance appears to be the most eﬀective andpractical method to control the canker. Valsa ceratosperma is
considered to be equally pathogenic on all cultivated apples(Sawamura et al. 1993); however, high resistance could bepresent in some Malus species and apple rootstocks (Liu et al.
1990, Bessho et al. 1994). The objective of this study was toevaluate resistance levels of diverse Malus species, accessions
and several apple cultivars to V. ceratosperma, using an
artiﬁcial inoculation test. Additionally some accessions, among
which a wide range of resistance exists, were tested against
diﬀerent isolates of V. ceratosperma originating from diﬀerent
districts of Japan.

Materials and Methods
Plant materials: Fifty-three accessions of Malus species and theirinterspeciﬁc hybrids originating from diﬀerent geographical locations
were inoculated with isolate AVC-12 of V. ceratosperma. The reportedly resistant accession M. sieboldii ÔSanashi 61Õ (Bessho et al. 1994)
was included as a resistant check and the ÔFujiÕ apple used as asusceptible check. Ten dormant shoots and 10 succulent growing
shoots for each accession were collected from trees in a ﬁeld of the
National Institute of Fruit Tree Science, Morioka, Japan in December
and July, respectively. One 12-cm segment was cut from the middle ofeach shoot and used in the excised shoot assay. Ten twigs for eachaccession were subjected to the inoculation test.
Inoculation and disease assessment: The monoconidial isolate AVC-12
of V. ceratosperma (Tode ex Fr.) Maire, originating from an infected
apple tree in Aomori Prefecture, Japan, was used. Isolates were
multiplied on potato dextrose agar medium for 14 days at 25°C in
darkness. The preparation of the inoculum and the method of
inoculation followed that developed by Suzaki et al. (1997) withminor modiﬁcations. After a 14-day incubation, fungal mycelium(2.1 · 10)2 g) was added into a 100 ml volume of sterilized water andthen mildly homogenized for about 30 s. The mixture after homogenization was used as an inoculum (concentration of mycelial solution:
2.1 · 10)4 g mycelium per ml) for the excised shoot assay. The distal
cut end of each twig segment was subjected to scorching with a ﬂat ironto kill the tissue at the surface of the distal cut end and to ensure easy
invasion by the hyphae of the inoculum into the twigs. After scorching,
10 twigs were tied up and placed vertically into a plastic box so that theproximal cut end of each bundle of twigs was about 1 cm deep in thewater. A droplet of 20 ll of the inoculum was dripped on to the distal
end of each twig at the site of scorching and then the plastic box was
immediately covered with a vinyl ﬁlm to retain the humidity of the
inoculated twigs. The twigs were kept in darkness at 25°C for 10 days
for the dormant shoot and 7 days for the growing shoot. As noninoculated controls, ﬁve twigs for each accession were prepared by thesame procedure described above, and a droplet of 20 ll of sterilized
water was put on to the distal end of each twig. These were also kept at
25°C in darkness in humid conditions in the plastic box covered withvinyl ﬁlm. The lesion length of the necrosis caused by the inoculum waswww.blackwell-synergy.com

450
measured at 10 days post-inoculation for the dormant shoot assay andat 7 days post-inoculation for the growing shoot assay. The noninoculated controls, which received sterilized water, exhibited novisible symptoms of necrotic lesions in the twigs.
Stability of resistance against V. ceratosperma: Seven Malus accessions, together with resistant and susceptible checks showing a wide
range in their degree of resistance, were evaluated with three diﬀerent
isolates. For each accession and isolate, 10–15 twigs were prepared forthe excised dormant shoot assay. Three isolates, AVC-12 and AVC-55,
originating from an infected apple tree in Aomori Prefecture, Japan,
and VC 96-A, originating from Iwate Prefecture, Japan, were used.

Results and Discussion
In the excised shoot assay, the susceptible control
Malus · domestica ÔFujiÕ had high values for necrotic lesion
lengths (21.3 mm in the dormant shoot assay and 25.1 mm in
the growing shoot assay, Table 1), whereas the resistant check
M. sieboldii ÔSanashi 61Õ showed the lowest values for lesion
lengths (mean length ¼ 4.6 and 4.8 mm in the dormant andgrowing shoots, respectively) among the Malus accessions. The
results using dormant shoots agree with those from a previous
study (Bessho et al. 1994), in which ÔFujiÕ was highly susceptible, while a few genotypes of M. sieboldii, including ÔSanashi
61Õ, possessed a high level of resistance to Valsa canker among
apple rootstocks and Malus germplasm collections tested using
dormant shoots. Twenty-eight of the ﬁfty-three Malus accessions studied, together with the resistant check ÔSanashi 61Õ,displayed lower values for lesions than the susceptible checkÔFujiÕ (Dunnet’s test at P ¼ 0.05) in the excised dormant shootassay. When the growing shoots were used for the inoculation
test, 26 accessions showed lower values for mean lesions thanÔFuji.Õ The results indicated that 23 of the 53 Malus accessions
had signiﬁcantly lower values for mean lesions than wereobserved in ÔFujiÕ (Dunnet’s test at P ¼ 0.05) regardless of thediﬀerence in the stage of growth (Table 1).
Though resistance studies have not been conducted withinoculations of V. ceratosperma using growing shoots, aninoculation test using an excised growing shoot appears to bereliable for the evaluation of the resistance level against
V. ceratosperma, as well as an inoculation test using excised
dormant shoots. These observations are based on the results
shown in Table 1. Most of the accessions in the growing shootassay, however, gave high values for mean lesion lengths incomparison with those of the dormant shoot assay, despite theshorter duration of post-inoculation in the growing shootassay. This tendency might suggest that the levels of resistanceof Malus plants to V. ceratosperma vary within diﬀerent kindof plant tissues, dormant shoots and succulent growing ones.
The change from actively-growing current shoots to dormant
ones in woody plants is characterized mainly by the ligniﬁcation on the growing shoots; the modiﬁcation of cell walls bylignin and/or suberin in plant tissue is generally thought tomake them more resistant to the compressive forces exerted bypathogens (Bostock and Stermer 1989). In this connection,
there are some reports that the ligniﬁcation of bark tissues isinvolved with resistance to canker-forming pathogens inwoody perennials (Doster and Bostock 1988, Simard et al.
2001). With regard to this study, ligniﬁcation in the dormant
shoots of Malus accessions might be associated with theincreased levels of resistance to V. ceratosperma. Further study
will be necessary to determine whether or not the degree ofA b e , K o t o d a , K a t o and S o e j i m a

resistance level to V. ceratosperma among diﬀerent kinds ofplant tissues is related to lignin and/or suberin formation.
The relative lesion length to the susceptible controlÔFujiÕ wasa useful parameter to diﬀerentiate between resistant andsusceptible accessions regardless of the diﬀerence in the stageof growth. The mean length of a lesion of an accession whose
relative length to ÔFujiÕ in dormant shoots (RLD) and that ingrowing shoots (RLG) had values greater than 0.7 was not
signiﬁcantly diﬀerent from that of ÔFujiÕ, whereas the lesion
value of an accession with an RLD and RLG below 0.6 was
statistically diﬀerent from that of ÔFujiÕ without exception(P < 0.01, Table 1). Fourteen accessions, M. baccataÔNikkozumiÕ, M. ﬂorentina, M. halliana ÔHanyaehanakaidoÕ
ÔNokaidoÕ ÔTarehanakaidoÕ, M. micromalus ÔHongHaiTangÕ,M. pratii, M. sieboldii ÔKobanozumiÕ ÔMo 15Õ ÔSanashi 61ÕÔSanashi 63Õ, M. yunnanensis ÔVeitchiiÕ, M. · ﬂoribunda and
M. · platycarpa gave low RLD and RLG values of less than 0.6
and were evaluated as resistant. Ten accessions, M. asiatica
ÔJiringoÕ ÔRinkiÕ, M. baccata ÔMokotoÕ, M. coronaria ÔBracteataÕ
ÔCharlottaeÕ, M. halliana ÔHanakaidoÕ, M. ioensis, M. kansuensisÔHeNanHaiTangÕ, M. sieversii and M. · arnoldiana had RLD
and RLG values of less than 0.7, and at least either the RLD or
RLG ranged from 0.6 to 0.7; these were classiﬁed as moderately
resistant. The remaining 29 accessions including major apple
cultivars had RLD and/or RLG values above 0.7 and wereregarded as susceptible.
Signiﬁcant diﬀerences in the degree of resistance to V. ceratosperma were observed among both Malus species and Malus
accessions. Interestingly, 7 of the 14 resistant accessions
belonged to either M. halliana or M. sieboldii, which originated in Japan and/or Korea (Way et al. 1990), the most
predominant districts for the occurrence of the Valsa canker inthe world for apple production. The highest level of resistance
was found in M. sieboldii among diverse Malus accessions. The
diﬀerence in the level of resistance within accessions belonging
to the same Malus species appears to reﬂect the fact that apples
are highly heterozygous, which is documented in several
isozyme or SSR analyses (Chevreau et al. 1985, Weeden andLamb 1987, Hokanson et al. 2001, Kitahara et al. 2005, Volket al. 2005, Guarino et al. 2006). As apples have a gametophytic self-incompatibility system that enforces outbreeding(de Nettancourt 1977), this probably generates high heterozygosity. As a result of this outbreeding, genetic diversity forresistance level to the Valsa canker within Malus accessions
from the same species has also been generated. All domestic
apple cultivars tested, on the contrary, were highly susceptible
to the Valsa canker. The scab-resistant ÔPrimaÕ and ÔLibertyÕ,having M. · ﬂoribunda as an ancestor and carrying Vf (Crosby
et al. 1992, Merwin et al. 1994, Durel et al. 2003), weresusceptible as well, although M. · ﬂoribunda itself was evaluated as resistant to the Valsa canker. However, some
Vf -resistant cultivars, such as ÔReleikaÕ and ÔReneÕ, arereported to be resistant not only to apple scab but also to
ﬁre blight and bacterial canker (Fischer 2000a,b, Richter andFischer 2000). Therefore, it may be worthwhile to investigate
resistance to the Valsa canker using disease-resistant apple
cultivars more extensively and not chosen for the inoculation
test in the current study.
There were high positive correlations between lesion lengths
caused by isolate AVC-12 and those caused by isolate AVC-55(r ¼ 0.995, P < 0.01). Similar ﬁndings apply to the lesion
lengths caused by isolate AVC-12 and those caused by isolate

Fuji
M. angustifolia
Daito 2
JiringoRinki
WaringoMandschurica 1
MokotoNikkozumi
ShanDingZi 1
ShanDingZi 3
BracteataCharlottae
M. ﬂorentina
ChuiSiHaiTang
Hanakaido
Hanyaehanakaido
NokaidoTarehanakaido
M. honanensis
HuBeiHaiTang 83051
M. ioensis
HeNanHaiTang
HongHaiTang
LiJiangHaiTang
M. pratii
Kobanozumi
Miyamakaido
MO 15
Sanashi 61
Sanashi 63
M. sieversii
M. sikkimensis
HaiTangHua
BianYeHaiTang 83034
Miyagi 1
M. yunnanensis
Veitchii
M. arnoldiana
M. ﬂoribunda 88071
M. gloriosa
M. hartwigii
M. platycarpa 73031
M. robusta Bailey
Robusta 5
Scheideckeri
M. soulardii

Accession

Origin1(Susceptible check)
North America
North China, Korea
North China, Korea
North China, Korea
North China, Korea
North China, Japan, Korea
North China, Japan, Korea
North China, Japan, Korea
North China, Japan, Korea
North China, Japan, Korea
North America
North America
Europe
Japan
Japan
Japan
Japan
Japan
Central China
Central China
North America
North-western China
South-eastern China, Korea
South-eastern China, Korea
South-western China
Japan, Korea
Japan, Korea
Japan, Korea
Japan, Korea (Resistant check)
Japan, Korea
North-western China
Himalaya
Not identiﬁed
Not identiﬁed
JapanSouth-western China
South-western China

Species

M. · domestica Borkh.
M. angustifolia Michx.
M. asiatica Nakai
M. asiatica Nakai
M. asiatica Nakai
M. asiatica Nakai
M. baccata Borkh.
M. baccata Borkh.
M. baccata Borkh.
M. baccata Borkh.
M. baccata Borkh.
M. coronaria Mill.
M. coronaria Mill.
M. ﬂorentina (Zucc.) Schneid.
M. halliana Koehn.
M. halliana Koehn.
M. halliana Koehn.
M. halliana Koehn.
M. halliana Koehn.
M. honanensis Rehd.
M. hupehensis Rehd.
M. ioensis Brit.
M. kansuensis Schneid.
M. micromalus Makino
M. micromalus Makino
M. pratii (Hemsl.) Schneid.
M. sieboldii Rehd.
M. sieboldii Rehd.
M. sieboldii Rehd.
M. sieboldii Rehd.
M. sieboldii Rehd.
M. sieversii (Lodeb.) Roem.
M. sikkimensis Koehn.
M. spectabilis Borkh.
M. toringoides Hughes.
M. tschonoskii Schneid.
M. yunnanensis Schneid.
M. yunnanensis Schneid.
M. · arnoldiana Sarg.
M. · ﬂoribunda Sieb.
M. · gloriosa Lemoine
M. · hartwigii Koehn.
M. · platycarpa Rehd.
M. · robusta Rehd.
M. · robusta Rehd.
M. · scheideckeri Zabel
M. · soulardii Brit.
21.3
16.0
18.0
13.1**
13.9**
16.5
15.3
13.2**
6.0**
12.9**
15.2
13.8**
14.5
7.0**
15.4
9.4**
12.0**
7.8**
10.5**
18.0
15.6
11.8**
13.7**
11.4**
20.6
11.0**
11.6**
13.4**
5.0**
4.6**
11.5**
14.0*
14.5
12.3**
11.0**
16.3
17.0
11.5**
14.1*
9.5**
15.8
16.8
9.8**
14.6
16.2
9.3**
15.4

Mean length oflesion (mm)Dormant shoot2

1.00
0.75
0.85
0.62
0.65
0.77
0.72
0.62
0.28
0.61
0.71
0.65
0.68
0.33
0.72
0.44
0.56
0.37
0.49
0.85
0.73
0.55
0.64
0.54
0.97
0.52
0.54
0.63
0.23
0.22
0.54
0.66
0.68
0.58
0.52
0.76
0.80
0.54
0.66
0.45
0.74
0.79
0.46
0.69
0.76
0.44
0.72

RLD

Table 1: Length of necrosis on excised shoots of diverse Malus accessions inoculated with a virulent isolate, AVC-12 of Valsa ceratosperma

25.1
16.1**
18.0
13.5**
15.7**
17.2*
18.0
16.9**
14.5**
18.6
17.4
15.4**
16.2**
11.0**
25.5
15.7**
11.2**
11.7**
12.2**
19.5
20.8
16.8**
13.2**
14.1**
24.4
11.0**
12.3**
23.3
5.8**
4.8**
10.2**
15.4**
19.0
19.0
19.1
20.3
19.6
14.9**
14.9**
9.4**
19.3
20.0
11.7**
20.5
24.3
18.3
20.0

Mean length oflesion (mm)Growing shoot2

1.00
0.64
0.72
0.54
0.63
0.69
0.72
0.67
0.58
0.74
0.69
0.61
0.64
0.44
1.02
0.63
0.45
0.46
0.49
0.78
0.83
0.67
0.52
0.56
0.97
0.44
0.49
0.93
0.23
0.19
0.41
0.61
0.76
0.76
0.76
0.81
0.78
0.59
0.59
0.37
0.77
0.80
0.47
0.82
0.97
0.73
0.80

RLG

Susceptible
Susceptible
Susceptible
Moderately resistantModerately resistantSusceptible
Susceptible
Moderately resistantResistant
Susceptible
Susceptible
Moderately resistantModerately resistantResistant
Susceptible
Moderately resistantResistant
Resistant
Resistant
Susceptible
Susceptible
Moderately resistantModerately resistantResistant
Susceptible
Resistant
Resistant
Susceptible
Resistant
Resistant
ResistantModerately resistantSusceptible
Susceptible
Susceptible
Susceptible
Susceptible
ResistantModerately resistantResistant
Susceptible
Susceptible
Resistant
Susceptible
Susceptible
Susceptible
Susceptible

Evaluation3

Resistance sources of Malus to Valsa canker
451

A b e , K o t o d a , K a t o and S o e j i m a

M. · domestica Borkh.
M. · domestica Borkh.
M. · domestica Borkh.
M. · domestica Borkh.
M. · domestica Borkh.
M. · domestica Borkh.
Gala
Golden Delicious
JonathanLibertyPrima
Starking Delicious

RLD: relative lesion length to ÔFujiÕ in dormant shoots (mean lesion length of the respective accession/21.3), RLG: relative lesion length to ÔFujiÕ in succulent growing shoots (mean lesion length of therespective accession/25.1).
1
Origin of the primary Malus species described by Way et al. (1990).
2
Dormant shoots were collected and inoculated in December, and growing shoots in July.
3
Susceptible: RLD > 0.70 or RLG > 0.70; moderately resistant: 0.60 £ RLD and/or RLG £ 0.70; resistant: RLD, RLG < 0.60.
*
and **differ signiﬁcantly from the susceptible check ÔFujiÕ (Dunnet’s test at P ¼ 0.05 and P ¼ 0.01).

Susceptible
Susceptible
Susceptible
Susceptible
Susceptible
Susceptible
1.03
0.80
0.98
0.79
0.93
1.03
25.8
20.1
24.6
19.9
23.4
25.9
0.84
0.80
0.98
0.87
0.86
1.11
17.8
17.0
20.9
18.5
18.3
23.7

Mean length oflesion (mm)Mean length oflesion (mm)
Accession

Table 1: Continued

Species

Origin1

Dormant shoot2

RLD

Growing shoot2

RLG

Evaluation3452

VC 96-A (r ¼ 0.985, P < 0.01), and the lesion lengths causedby isolate AVC-55 and those caused by isolate VC 96-A (r ¼
0.990, P < 0.01) when nine accessions from diverse Malus
species showing a wide range in their degree of resistance were
tested for the excised dormant shoot assay (data not shown).
Although little is known about the speciﬁc interaction between
Malus genotypes and isolates of V. ceratosperma, the results
suggested that there was no evidence for the existence ofspeciﬁc races virulent to M. sieboldii.
Clearly, several accessions from M. sieboldii, M. halliana,
M. ﬂorentina and M. · ﬂoribunda were demonstrated to possess a good level of resistance against V. ceratosperma; ÔMo 15Õand ÔSanashi 61Õ from M. sieboldii were evaluated and found tohave a particularly high level of resistance, which makes them
useful as breeding materials for resistance breeding against the
Valsa canker. In the process of selecting resistant plants
against V. ceratosperma in the progenies derived from theresistant Malus species mentioned above, the values of therelative lesion length to the susceptible control ÔFujiÕ areacceptable as a simple but reliable parameter. To date, anumber of Malus species have been used worldwide to improvecertain traits in the cultivated apple. As a result, it was foundthat interspeciﬁc hybridizations between cultivated apples anda wide range of Malus species was successful (Korban 1986,
Bus et al. 2000, Fischer et al. 2003). Among the resistantMalus species against Valsa canker, M. sieboldii is known topossess the highest level of resistance to ﬁre blight (Gardneret al. 1980) and powdery mildew (Schuster 2000), M. ﬂorentina
is resistant to powdery mildew (Schuster 2000), and families
originating from M. baccata are resistant to ﬁre blight(Gardner et al. 1980, Luby et al. 2002); consequently a longterm apple breeding programme for multiple disease resistancecan be justiﬁed using a resistant accession as a parent.
The strong focus of the resistance breeding programme iscurrently put on resistance to scab (Venturia inaequalis), as is
the case in the apple-breeding programme at the National
Institute of Fruit Tree Science (NIFTS) in Japan. In thisconnection, new scab-resistant cultivars with attractive fruit
appearance and/or quality (e.g. Fischer 2000a, Janick et al.
2004a,b, Khanizadeh et al. 2003, Korban et al. 2003, Laurens
et al. 2005) are worthwhile not only for testing their ﬁeld
performance in the environmental conditions at several apple
production districts in Japan but also for consideration as
parents in future breeding at NIFTS to develop dessert apple
cultivars with multiple resistance.
Acknowledgements
The authors thank Dr K. Suzaki for providing the V. ceratosperma
isolates used in this study.

References
Bessho, H., S. Tsuchiya, and J. Soejima, 1994: Screening methodsof apple trees for resistance to Valsa canker. Euphytica 77,
15—18.
Bostock, R. M., and B. A. Stermer, 1989: Perspectives on woundhealing in resistance to pathogens. Annu. Rev. Phytopathol. 27,
343—371.
Brown-Rytlewski, D. E., and P. S. McManus, 2000: Virulence ofBotryosphaeria dothidea and Botryosphaeria obtusa on apple andmanagement of stem cankers with fungicides. Plant Dis. 84,
1031—1037.

Resistance sources of Malus to Valsa canker
Bus, V., S. Bradley, M. Hofstee, P. Alspach, L. Brewer, and J. Luby,
2000: Increasing genetic diversity in apple breeding to improve thedurability of pest and disease resistance. Acta Hortic. 538, 185—190.
Chevreau, E., Y. Lespinasse, and M. Gallet, 1985: Inheritance ofpollen enzymes and polyploid origin of apple (Malus · domestica
Borkh.). Theor. Appl. Genet. 71, 268—277.
Crosby, J. A., J. Janick, P. C. Pecknold, S. S. Korban, P. A. O’Connor,
S. M. Ries, J. Goﬀreda, and A. Voordeckers, 1992: Breeding apples
for scab resistance: 1945–1990. Fruit Var. J. 46, 145—166.
Doster, M. A., and R. M. Bostock, 1988: Effects of low temperatureon resistance of almond trees to Phytophthora pruning woundcankers in relation to lignin and suberin formation in wounded barktissue. Phytopathology 78, 478—483.
Durel, C. E., L. Parisi, F. Laurens, W. E. Van de Weg, R. Liebhard,and M. F. Jourjon, 2003: Genetic dissection of partial resistance torace 6 of Venturia inaequalis in apple. Genome 46, 224—234.
Fischer, C., 2000a: Apple breeding in the Federal Centre for Plant
Breeding Research, Institute for Fruit Breeding at Dresden-Pillnitz,
Germany. Acta Hortic. 538, 225—227.
Fischer, C., 2000b: Multiple resistant apple cultivars and consequences
for apple breeding in the future. Acta Hortic. 538, 229—234.
Fischer, M., M. Geibel, and R. Büttner, 2003: Zwischen ÔAnacuta’undÔPinovaÕ- Bilanz 10-jahriger Genbankarbeit für Obst in DresdenPillnitz. Erwerbsobstbau 45, 22—29.
Gardner, R. G., J. N. Cummins, and H. S. Aldwinckle, 1980: Fire
blight resistance in the Geneva apple rootstock breeding program.
J. Am. Soc. Hortic. Sci. 105, 907—912.
Guarino, C., S. Santoro, L. De Simone, O. Lain, G. Cipriani, and R.
Testolin, 2006: Genetic diversity in a collection of ancient cultivarsof apple (Malus·domestica Borkh.) as revealed by SSR-based
ﬁngerprinting. J. Hortic. Sci. Biotechnol. 81, 39—44.
Hokanson, S. C., W. F. Lamboy, A. K. Szewc-McFadden, and J. R.
McFerson, 2001: Microsatellite (SSR) variation in a collection ofMalus (apple) species and hybrids. Euphytica 118, 281—294.
Janick, J., J. C. Goﬀreda, and S. S. Korban, 2004a: ÔCo-op 29Õ (Pixie
CrunchTM) apple. HortScience 39, 450—451.
Janick, J., J. C. Goﬀreda, and S. S. Korban, 2004b: ÔCo-op 33Õ
(SundanceTM) apple. HortScience 39, 452—453.
Khanizadeh, S., F. Laurens, Y. Lespinasse, Y. Groleau, J. Cousineau,
O. Carisse, and J. DeEll, 2003: ÔGalarinaÕ apple. HortScience 38,
477—478.
Kitahara, K., S. Matsumoto, T. Yamamoto, J. Soejima, T. Kimura, H.
Komatsu, and K. Abe, 2005: Molecular characterization of apple
cultivars in Japan by S-RNase analysis and SSR markers. J. Am.
Soc. Hortic. Sci. 130, 885—892.
Korban, S. S., 1986: Interspeciﬁc hybridization in Malus. HortScience21, 41—48.
Korban, S. S., C. Goﬀreda, and J. Janick, 2003: ÔCo-op 43Õ (JulietTM)
apple. HortScience 38, 144—145.
Laurens, H., Y. Lespinasse, and A. Fouillet, 2005: A new scabresistant apple: ÔArianeÕ. HortScience 40, 484—485.

453
Liu, H. Z., Q. M. Ren, and L. J. Liu, 1990: Evaluation of resistance to
Valsa mali in Malus germplasm resources. J. Fruit Sci. 7, 65—70.
Luby, J. J., P. A. Alspach, V. G. M. Bus, and N. C. Oraguzie, 2002:
Field resistance to ﬁre blight in a diverse apple (Malus sp.)
germplasm collection. J. Am. Soc. Hortic. Sci. 127, 245—253.
Merwin, I. A., S. K. Brown, D. A. Rosenberger, D. R. Cooley, andL. P. Berkett, 1994: Scab-resistant apples for the northeastern
United States: new prospects and old problems. Plant Dis. 78,
4—10.
de Nettancourt D., 1977: Incompatibility in Angiosperms. Monographs on Theoretical and Applied Genetics, Vol. 3. SpringerVerlag, Heidelberg, Germany.
Richter, K., and C. Fischer, 2000: Stability of ﬁre blight resistance inapple. Acta Hortic. 538, 267—270.
Sakuma, T., 1990: Valsa canker. In: A. L. Jones, and H. S. Aldwinckle(eds), Compendium of Apple and Pear Diseases, 39—40. APS Press,
St Paul, USA.
Sawamura, K., Y. Harada, and K. Yukita, 1990: Apple Valsa canker
caused by Valsa ceratosperma (Tode: Fr.) Maire. Bull. Fac. Agric.
Hirosaki Univ. 53, 10—32.
Sawamura, K., Y. Harada, T. Kikuchi, and J. M. Ogawa, 1993: The
apple industry in Japan. A historical sketch and diseases speciﬁc to
the region. Plant Dis. 77, 546—552.
Schuster, M., 2000: Genetics of powdery mildew resistance in Malus
species. Acta Hortic. 538, 593—595.
Simard, M., D. Rioux, and G. Laﬂamme, 2001: Formation of lingosuberized tissues in jack pine resistant to the European race ofGremmeniella abietina. Phytopathology 91, 1128—1140.
Suzaki, K., K. Yoshida, and T. Ito, 1997: Pathogenicity to apple
branch and phloridzin degrading activity of Valsa ceratosperma
isolated from some broad leaf trees including apple tree. Annu.
Rept. Plant Prot. North Japan 48, 145—147.
Tamura, O., and I. Saito, 1982: Histopathological changes of apple
bark infected by Valsa ceratosperma (Tode ex Fr.) Maire during
dormant and growing periods. Ann. Phytopathol. Soc. Japan 48,
490—498.
Uhm, J. Y., and H. R. Sohn, 1995: Control of apple Valsa canker by
localized spraying with neoasozin solution, an arsenic fungicide.
Korean J. Plant Pathol. 11, 9—16.
Volk, G. M., C. M. Richards, A. A. Reilley, and A. D. Henk, 2005: Exsite conservation of vegetatively propagated species: development of
a seed-based core collection for Malus sieversii. J. Am. Soc. Hortic.
Sci. 130, 203—210.
Way, R. D., H. S. Aldwinckle, R. C. Lamb, A. Rejman, S. Sansavini,T. Shen, R. Watkins, M. N. Westwood, and Y. Yoshida, 1990:
Apples (Malus). In: J. N. Moore, and J. R. Ballington Jr (eds),
Genetic Resources of Temperate Fruit and Nut Crops, 3—62. Int.
Soc. Hortic. Sci., Wageningen, the Netherlands.
Weeden, N. F., and R. C. Lamb, 1987: Genetics and linkage analysis
of 19 isozyme loci in apple. J. Am. Soc. Hortic. Sci. 112, 865—872.