The Planter, Kuala Lumpur, 87 (1024): 515-526 (2011)

Ganoderma boninense in Oil Palm Plantations:

Current Thinking on Epidemiology, Resistance
and Pathology*
COOPER, R Ma, J FLOODb, AND R W REESa

This review addresses some key current issues concerning Ganoderma boninense, causal agent of basal
stem rot (BSR) and upper stem rot (USR), as a continuing limiting factor in palm oil production. Spread
and infection can occur through roots, yet genetic evidence shows considerable isolate diversity and
reveals the major input of airborne basidiospores to spread and infection. This has implications for control
measures, screening for resistance and choice and deployment of resistance. Where infective heterokaryotic
mycelium resulting from spore matings establishes or infects is not understood, because Ganoderma is a
weak saprophytic competitor in soil and palm debris. Spores do germinate on cut fronds (and on other
wounded surfaces, as revealed by cryo-scanning electron microscopy) and are pulled into xylem vessels
under negative tension and may colonise from that protected niche. Improved screening for resistance by
attaching small inoculum to roots, along with shading seedlings to mimic canopy cover are described.
Pathogenicity mechanisms of G. boninense revealed by light and transmission electron microscopy involves
an initial biotrophic phase in root cortex and lower stem, rapid starch depletion then extensive, simultaneous
host cell wall breakdown by its array of lignases and polysaccharidases.
Suggestions for future research are outlined.

Keywords: Basidiospores, white rot, tetrapolar mating, DNA markers, cell wall degradation, hemibiotrophy,
root infection, starch degradation, resistance.

Basal stem rot (BSR) incidence caused by the Africa, Papua New Guinea and Thailand (Idris
basidiomycete, white rot, fungal pathogen et al., 2004). Lim et al. (1992) recorded in
Ganoderma boninense continues to increase Malaysian coastal areas an average of 50 per
in oil palm plantings, and is to be expected with cent yield losses from 80 per cent of 13-year-
such large scale monoculture (Turner, 1981). old plantings. However, diseased palms as
Basal stem rot (BSR) involves decay of the young as 12-24 months after planting can occur
lower stem and sometimes the root system, (Singh, 1991). Although the disease is well
leading to severe symptoms such as flattening established in Malaysian coastal areas, Rao et
of the crown and unopened spear leaves al. (2003) reported typical levels of disease
(Figure 1). Most severe losses from BSR incidence of 30 per cent on 13-year-old palms
occur in mature stands in Indonesia and in both inland and peat soils. In North Sumatra,
Malaysia with lower incidences recorded in the location of the fieldwork described herein,
a
Department of Biology and Biochemistry, University of Bath, Claverton Down, Bath, BA2 7AY,
United Kingdom.
b
CABI Europe-UK, Bakeham Lane, Egham Surrey, TW20 9AY, United Kingdom.
* Paper presented at the seminar/dialogue titled Sustainable Agriculture - An Insight into Ganoderma
held on 24 February 2011 in Kuala Lumpur organised by Agrinos Sdn Bhd.

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Ganoderma boninense in oil palm plantations: current thinking on epidemiology, resistance and pathology

on average was 0.16 tonnes per hectare fresh

Figure 1 Symptoms of Ganoderma with
BSR in Sumatra
at the time of replanting (25 years) 40-50 per
cent of palms are lost with the majority of
standing palms showing disease symptoms.
Losses begin to have a financial effect once
the disease affects more than 10 per cent of
the stand (Hasan & Turner, 1998). Yield decline
fruit bunch (FFB) for every palm lost, and
when the stand had declined by 50 per cent
mean losses were c. 35 per cent (Subagio &
Foster, 2003).
Young palms, once infected usually die
within 6-24 months after the first appearance
of symptoms, whereas mature palms survive
for 2-3 years or more. Initial disease can be
difficult to diagnose, and the pathogen can be
present in symptomless, naturally infected
mature trees (Corley & Tinker, 2003). One
definitive diagnostic feature of the disease in
standing palms is the presence of characteristic
basidiocarps on the stems of infected palms
(Figure 2). Basal stem rot, which manifests
as a decay of the bole leading ultimately to the
toppling of the palm, is the most frequently
observed G. boninense infection. The
occurrence of upper stem rot (USR) where
decay occurs higher up the stem (above 1-
1.5 metres) and can cause palms to break in
two, is much less frequent. The two symptoms
are usually physically separated and the result
of different infection events. In severe
infections, stem fracture can result (Hasan et

Figure 2 Left to right: Typical basidiocarps of G. boninense from a BSR affected palm; we detected 14,000
spores/min from one fruiting body of 10 cm2. Diurnal fluctuation of aerial basidiospore numbers
in a 17 year old plot in N Sumatra. Error bars are SD of 4 replicate samples

516

al., 2005; Pilotti, 2005; Rees et al., 2007).
Ganoderma exists in the field as mycelium
colonising palm tissue, as abundant fruiting
bodies (basidiocarps) and as myriad mono-
karyotic basidiospores. Monokaryotic mycelium
from basidiospores can colonise palm wood but
is non-infective (Hasan & Flood, 2003; Rees
et al., 2007); anastomosis with a compatible
mating type is required to form the potentially
invasive and faster growing heterokaryon.
This overview will focus on a few current
aspects of Ganoderma stem rots. Control
strategies are dealt with in an accompanying
paper.
RESULTS AND DISCUSSION
Mode of infection and epidemiology
Elucidating the route of infection and extent of
pathogen diversity is crucial in order to enable
development of successful management
practices for disease control. This remains a
controversial area and one that needs careful
resolution.
Root infection
BSR can result from root infection, presumably
following root contact with soil inoculum or
other infected roots. Rees et al. (2007; 2009)
Figure 3 Left to right: natural infection of multiple palm roots. Roots have been excised to show the many
necrotic lesions at the base of the bole. Inoculation of a seedling palm root by attaching a 3x3x3
cm rubber wood block colonized by G. boninense. Stem lesion developing from two inoculated
roots.
The Planter, Vol. 87, No. 1024, July 2011
clearly showed that controlled root infection
leads to typical symptoms. Numerous infection
trials using oil palm seedlings and often large
Ganoderma-colonised rubberwood blocks
have provided data supporting this view
(Navaratnam & Chee, 1965; Lim et al., 1992;
Sariah et al., 1994; Hasan & Turner, 1998; Lim
& Fong, 2005; Breton et al., 2006). Rees et
al. (2007) showed that by attaching
Ganoderma-infested wood blocks to roots
much smaller inoculum can be used, allowing
infection to occur through unwounded roots and
progression and rate of invasion to be followed.
Other evidence indicating root infection
from the field comes from Rees et al. (2007)
who showed multiple, natural infections of
different roots in a single palm (Figure 3).
Infection of seedlings resulted from nearby
colonised oil palm, with those seedlings nearer
to the colonised trunks becoming diseased more
quickly (Flood et al., 2005). Hasan and Turner
(1998) also showed seedlings become infected
when planted near infected stumps (from the
previous planting). Infection resulting from
colonised debris or from windrows remaining
in the field at replanting is suggested by the
reduced infection observed in subsequent
replantings following fallowing and various
windrow treatments (Virdiana et al., 2010).
517
Ganoderma boninense in oil palm plantations: current thinking on epidemiology, resistance and pathology
Additionally, increased incidence of infection
is seen following poor land preparation at
replanting time with infected boles left in the
ground (H. Foster, pers. comm.). Oil palm roots
from mature palms can extend up to four
planting rows, so root contact will be frequent
(Miller et al., 1999). Root infection occurs by
several other root-infecting basidiomycete
diseases of trees and perennial crops, which
are spread by vegetative growth, often as a
single genet, such as Heterobasidion annosum
and Armillaria mellea (Woodward et al.,
1998).
Rees et al. (2009) showed colonisation by
G. boninense can occur through unwounded
roots then progresses mainly through the inner,
thin-walled cortex. In contrast to previous work,
no initial colonisation was observed in the
vascular tissue, or lacunae (lacunae are wide,
long, axially orientated cylindrical spaces
surrounded by thin-walled cells) and prima
facie offer an ideal route for longitudinal spread,
but these channels were not exploited.
Crucially, we found that Ganoderma
required intimate contact with palm roots in
order to infect. This probably reflects two key
aspects of its biology. Firstly, it is a relatively
weak pathogen requiring a very large inoculum
to launch an attack. Secondly, it is a poor
competitor against other saprotrophic
microflora. This was evident by its virtual
inability to spread as mycelium from a nutrient
base in plantation soil or in the organic debris
that accumulates at frond bases. Growth did
occur once these substrates had first been
sterilised (Rees et al., 2007). This weak ability
to compete would preclude the possibility
of sufficient build-up of saprotrophic
G. boninense inoculum in soil or frond debris
to initiate infections or growth away from a
diseased root. Therefore it seems unlikely that
upper stem rot arises from colonisation of the
518
debris found in the axils of frond bases, and
that for BSR infection to occur, palm roots need
to contact inoculum rather than mycelium of
G. boninense actively contacting host roots.
Role of basidiospores
In contrast to the mode of infection described
above, others have questioned the involvement
of root infection (Ariffin et al., 1996; Miller et
al. 1999; Pilotti et al., 2003). Genetic studies
of G. boninense from infected palms in Papua
New Guinea (PNG) and Malaysia reveal
considerable diversity in oil palm plantations
according to mitochondrial DNA markers,
mating alleles and somatic (or vegetative)
compatability (Miller et al., 1999; Pilotti et al.,
2004; Pilotti, 2005). Different genotypes must
have arisen through sexual recombination then
dispersal via spread of basidiospores. Pilotti et
al. (2000) using Random Amplification of
Polymorphic DNA (RAPDs) revealed
considerable diversity in monokaryons, such
that each showed a unique RAPD genotype.
Also, outbreaks of BSR in new plantations
where G. boninense inoculum is not present
in debris or soil, implies introduction by spores
(Sanderson et al., 2000). Outcrossing is
favoured because G. boninense is heterothallic
and tetrapolar with multiple alleles at both mating
type loci (Pilotti et al., 2002).
Recently the study of G. boninense genetic
diversity by molecular characterisation, using
randomly amplified microsatellites (RAMS) as
nuclear DNA markers, of isolates from BSR
and USR infections and from isolates taken
from fallen palms (those killed and left within
established plantations) was extended in five
locations in North Sumatra (Rees et al., 2011).
Sumatra potentially offers a different pathogen
population from Malaysia and PNG. Also for
the first time, we determined quantitatively
basidiospores in plantation air.
 The Planter, Vol. 87, No. 1024, July 2011

Basidiospores were produced in prolific
numbers (2-11,000 /m3) throughout the 24 hour
sampling periods, with maximal release in the
evening (Figure 2). Clearly there will be
constant potential inoculum to colonise wounds
and palm debris throughout the plantation.
RAMS data largely agree with the high
isolate diversity in BSR (Figure 4). Thus three
of seven affected palms contained more than
one genotype of G. boninense. Miller et al.
(1999) similarly showed showed six out of eight
BSR infected palms in Malaysia yielded isolates
with different somatic compatibilities and
mtDNA RFLP profiles. Pilotti (2005) also found
multiple isolates in single palms. These results
clearly show predominantly multiple infections
rather than clonal spread. However, clonal
colonisation can occur, as revealed by all seven
isolates from a single BSR infected palm with
an identical RAMS profile (Rees et al., 2011).
Evidence for mycelial spread of the disease
between fallen palms or BSR palms was not
evident in our study. No RAMS profiles linked
BSR infected trees to neighbouring fallen palms
and none of the band patterns was shared
between isolates obtained from adjacent fallen
palms.
Nevertheless, analysis of isolates from
within two adjacent BSR palms did have
identical profiles. Likewise Miller et al. (2000)
found adjacent BSR palms contained isolates
with the same mtDNA RFLP band pattern and
Pilotti (2005) found 2 of 15 isolates from
adjacent palms with the same somatic
compatability. Therefore vegetative spread of
the pathogen does occur.
Cluster analysis conducted on the binary
matrix produced from banding patterns showed
that isolates from a single plot often did not
cluster together more than those from different
plantings or even from a different estate
>20 km distant (Rees et al., 2011). These data
agree with the high genetic variability observed
within oil palm cropping systems in Malaysia
and PNG (Miller et al.1999; Pilotti et al. 2003).
Migration of spores from outside planting areas
presumably explains how new alleles are being
detected every year (Pilotti, 2005).

Figure 4 Typical RAMS fingerprints of isolates from USR affected

palm and from fallen palms. Each lane results from a PCR
amplification. 100bp ladder to calculated band sizes is
shown on left & right side of the gel. Note variability
between isolates

519
Ganoderma boninense in oil palm plantations: current thinking on epidemiology, resistance and pathology

The role of spores in infection would also
be suggested by random distribution of disease,
rather than expanding clustered patterns of
spread as would be predicted from root to root
spread. Recent GPS positioning of BSR in
plantations in Sabah shows mostly random
distribution of BSR in several estates (N.
Hisham, pers. comm.). There are no reports
other than from Singh (1991) on clustering,
although some field observations might suggest
otherwise (G S Thind, pers. comm.).
Extensive wound sites are created by
routine harvesting (severing the fruit bunch
peduncle) and pruning (of frond base to free
the fruit bunch), so the potential for spore
infection is very considerable. Also trunk
wounds are more likely in older palms as
harvesting becomes more difficult at greater
height. Other vulnerable sites could be created
by mechanical damage from invertebrate pests
such as Oryctes rhinoceros and rats. Rees et
al. (2011) show for the first time that
basidiospores can germinate abundantly on cut
surfaces (fronds, peduncles, stem) under
plantation conditions. Spores contaminating the
surface of cut fronds are withdrawn up to
10 cm into xylem as a result of negative tension
within functional vessels (Cooper, 1981)
(Figure 5). Here, basidiospores would be
relatively protected from microbial competition,
dehydration and solar radiation. Anastomosis
was apparent in situ from our cryo-scanning
electron microscopy images concurring with
the observation that in vitro spores readily mate
(Pilotti, 2005). Formation of a resulting
heterokaryon, a prerequisite for formation of
infective mycelium, could conceivably result in
colonisation of vascular tissues extending into
the palm trunk.
Infection via wounded surfaces of fronds
was initially suggested by Thompson (1931).
Sanderson and Pilotti (1997) cut back the rachis
of decayed frond bases and followed lesions
into the stem base. They suggested that when
the palm expands, this initial infection would
appear to have originated near the centre of
the palm base, even though it arose from
the rachis possibly via connecting vascular
bundles. Infection of wounded frond surfaces
can occur according to Lim et al. (1992), but
G. boninense-colonised wheat-oat grain
medium was used as the inoculum source. In
contrast, Hasan et al. (2005) failed to reproduce
USR, using spores and even Ganoderma-
infested rubberwood.
Overall the data show a genetically variable

Figure 5 Cryo-scanning electron microscopy (left) showing basidiospore germination within

frond xylem vessels. Spores were applied to newly cut frond bases under plantation
conditions. Germinating pigmented basidiospores by light microscopy (right)

520

population in North Sumatra, Malaysia and
PNG and the importance of basidiospores in
spread and infection. However there are some
anomalies that need addressing.
Anomalies
All attempts to infect mature palms and
seedlings with basidiospores have failed (Hasan
et al., 2005; Idris pers. comm; Thompson,
1931; Turner, 1981; Yeong, 1972 cited in Miller
et al., 2000). This presumably reflects the
relatively low aggressiveness of G. boninense
and the requirement for a substantial source
of inoculum, as discussed by Rees et al. (2007).
Also as previously described, Rees et al. (2007)
revealed the very weak, competitive
saprotrophic ability of G. boninense in soil and
in organic debris. Therefore the question arises
as to where a heterokaryon might form and
flourish to create a sufficient inoculum.
Resistance and screening for resistance
Resistant varieties hold the greatest hope for
future control of BSR in oil palm in South East
Asia. Field observations in North Sumatra
revealed E. guineensis of deli origin from
Malaysia and Indonesia was more susceptible
Figure 6 Effect of shading on artificial infection of oil palm seedlings (left). Effect of temperature on
growth of G. boninense on agar (right); note that no growth would have occurred in the
temperatures attained in non-shaded soil of e 40 C
The Planter, Vol. 87, No. 1024, July 2011
than African material (Durand-Gasselin et al.,
2005), and other trials have revealed differences
in susceptibility, indicating possible genetic
resistance within host populations (Idris et al.,
2004; Breton et al., 2006; Durand-Gasselin,
pers. comm., 2011)
Use of a robust (reproducible, statistically
valid) and facile screening system for
evaluating performance of oil palm genotypes
is crucial. The methods using Ganoderma-
infested wood block inoculum were detailed
by Rees et al. (2007). In summary, rubber-
wood is superior to palm wood and direct
contact with inoculum gives faster and more
reliable infection and allows use of smaller
inoculum, saving time and space (Figure 6).
There is current investigation to source an
alternative to rubberwood as it is currently less
available.
It was shown by Rees et al. (2007) that
shading has a dramatic effect on disease, with
much earlier symptoms and significantly higher
levels of infection in shaded seedlings compared
to exposed palms (Figure 6). Shading is now
used routinely by many organisations. Flood et
al. (1993-unpublished) uncovered a similar
situation in Zaire (DRC) when screening for
resistance to Fusarium wilt. Soil temperatures
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Ganoderma boninense in oil palm plantations: current thinking on epidemiology, resistance and pathology

in exposed palms regularly exceeded 40C but
in vitro fungal growth was severely impaired
above 35C (growth optimum is c. 28C) and
two days exposure to 45C (the maximum
recorded) was lethal (Rees et al., 2007)
(Figure 6). This effect of temperature is likely
to explain the late appearance of G. boninense
infections in plantations. Losses in young
plantings are typically low, with field symptoms
only becoming apparent after about 10-12 years
and becoming financially significant after about
15 years (Rao et al., 2003). BSR has
incorrectly been described as a disease of
senescing palms. Ambient temperatures at soil
level would only favour build-up of active
G. boninense inoculum after the canopy was
fully formed. It is probable that older palms
are not especially susceptible to G. boninense-
infection, but rather altered environmental
conditions following canopy closure favour
BSR development. Routine artificial infection
of seedlings makes clear that infection can
occur throughout the growth cycle.
The genetics and nature of resistance or
tolerance shown by palms to Ganoderma is
not known and will await the availability of palm
lines with effective resistance. Typical defence
responses of woody tissues, such as reinforce-
ment of cell walls by suberinisation and/or
lignification or periderm formation were not
evident ultrastructurally in roots or stems (Rees
et al., 2009). Various preliminary molecular
studies have investigated up-regulation of
defence-related genes, but these are typical of
most plant species.
Pathogenicity
Root infection by G. boninense appears to
involve developmental switches (Rees et al.,
2009). There was an initial apparent biotrophic
phase in infection of both root cortex and stem
base, involving mainly intracellular colonisation
by wide hyphae in host cells which still
possessed fully intact cell walls and in some
cases contained recognisable cytoplasm
(Figure 7). This mode of invasion is
reminiscent of the well-characterised
hemibiotrophic phase of some ascomycetes
such as Colletotrichum spp. (Perfect et al.,

Figure 7 Nectrotrophic growth in root cortex with extensive host cell wall
destruction (left). Subtle intracellular growth by wide hyphae within
host cells in lower stem (right); this was followed by necrosis and wall
breakdown. Transmission electron microscopy.

522

1999). The biotrophic phase of invasion was
followed by an aggressive necrotrophic stage
associated with extensive host cell wall
degradation (Figure 7). A possible third phase
was the formation of melanised mycelium both
within host tissues (possibly in response to host
defences) and on a much larger scale external
to roots in the form of very tough pseudo-
sclerotia.
For successful penetration and degradation
of intact roots, production of an array of cell
wall-degrading enzymes (CWDE) (Cooper,
1984) is likely to be required in order to penetrate
the outermost tissues, comprising the
recalcitrant polymers cellulose, lignin and
suberin. Enzyme activities from G. boninense
corresponding to lignin and all other major
structural cell wall polymers were detected
together with their effect on host wall
composition during G. boninense infection
(Rees, 2006). One month after inoculation
bleaching on roots was evident beneath
adhering mycelium probably reflecting the
oxidative breakdown of lignin and the white
rot status ascribed to this genus (Adaskaveg
et al., 1990; Paterson, 2007). Invasion of root
cortex and stem parenchyma resulted in
development of holes through all cell wall layers
indicative of simultaneous cell wall attack, as
described for some other wood-degrading fungi
(see Rees et al., 2009). This contrasts with
selective lignin degradation, evident ultra-
structurally by the loss of electron density from
the middle lamella, with less degradation of the
polysaccharide components of the S1 and S2
cell wall layers (Agosin et al., 1990). Cell wall
attack was sometimes not adjacent to
G. boninense hyphae as is often associated
with the oxidative nature of lignin degradation
(Kirk, 1987). Manganese peroxidase (MnP)
and laccase production have been reported for
G. lucidum by dSouza et al. (1996). Also
The Planter, Vol. 87, No. 1024, July 2011
laccases can contribute to melanin formation,
as occurs in pseudo-sclerotia (Johansson et al.,
1999).
Starch represents another major
polysaccharide that appears to be utilised as a
significant source of carbon during BSR. The
very high starch content of oil palm seedlings
was rapidly depleted during early infection
(Rees, 2006) and was confirmed by
transmission electron microscopy of bole
tissues. G. boninense readily utilises insoluble
starch in vitro.
Analysis of putative pathogenicity factors
in this poorly understood and difficult
pathosystem should benefit from the targeted
inoculum method described by Rees et al.
(2007) which allowed for temporal microscopic,
biochemical and molecular studies of early host-
pathogen interactions. The method should also
enable a study equivalent to that described by
Karlsson et al. (2003) for H. annosum. In
this research more than 900 expression
sequence tags (ESTs) from total ribonucleic
acid (RNA) from mycelium during early
infection of Scots pine roots were obtained.
Such an analysis with Ganoderma would be
enhanced by the existing genome sequence
from the lignocellulose-degrading basidio-
mycete Phanerochaete chrysosporium
(Martinez et al., 2004) and the forthcoming
genome sequence of G. boninense itself.
CONCLUSIONS AND QUESTIONS
It is clear that there is a long way to go before
we understand enough of this complex disease
in order to contain it effectively. Funding for
targeted research should be given priority.
Researchers need to avoid polarisation of views
and consider the likely various ways that
Ganoderma operates as a pathogen. Disease
resistance, if it proves to be effective and
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Ganoderma boninense in oil palm plantations: current thinking on epidemiology, resistance and pathology
durable, is the key solution. Molecular
technologies, such as marker assisted selection
and linked resistance gene analogues with
quantitative trait loci (QTL) for resistance, can
be linked in once resistance to G. boninense is
clearly shown. As stated earlier, a reliable,
robust and realistic method of inoculation for
screening is fundamental. In the meantime, the
other control practices to reduce inoculum at
replanting, as outlined in another paper in June
issue of The Planter (Cooper, 2011) should be
followed.
Biological control, such as using
Trichoderma spp. has not been considered in
this paper for reasons of space. However, I
will add the cautionary note, that screening such
microbial agents in vitro on agar for antagonism
vs Ganoderma has limited value. More robust
information can be achieved using substrates
such as palm wood (unpublished data).
Persistence in soil is another critical criterion,
but arguably most important of all is persistence
in the rhizosphere and especially actual
colonisation of the root cortex, which some
Trichoderma isolates can achieve. From this
location Trichoderma can potentially limit root
infection by Ganoderma and prime host
defences and possibly continually colonise
newly formed and elongating palm roots.
Without these attributes, protection is unlikely
to extend beyond the seedling stage.
Based on various studies on G. boninense
diversity, which implicate basidiospores directly
and indirectly in stem rots, it seems clear that
management strategies should consider routine
removal of basidiocarps. This procedure is
already in place in PNG (Hunt & Pilotti, 2004);
Ganoderma stem rot has yet to become a
major problem in PNG, making this task more
achievable. However reduction of inoculum
and pathogen variation is also desirable in
Malaysia and Indonesia where BSR is a
524
serious constraint and USR incidence is
increasing, but the removal of basidiocarps in
these second and third generation estates might
in some areas be impracticable.
There are some outstanding questions
which should be addressed.
Can spores infect directly? Are cut fronds
the main infection site? What is the distance
that viable basidiospores can be carried in air
currents to establish new infections? What
substrates in plantations can heterokaryons
colonise from mated spores to form an inoculum
sufficient to achieve infection? Why does
Ganoderma infection vary considerably
between regions? Are some soils suppressive?
Will the enormous diversity of G. boninense
isolates prove to be a problem once resistant
or tolerant palm lines begin to be used on a
large scale? Will the resistance being reported
currently at seedling level translate into mature
palms under plantation conditions? How will it
operate? Will it express as resistance or
tolerance to G. boninense?
ACKNOWLEDGEMENTS
We wish to acknowledge funding from Biology
& Biotechnology Science Research Council
(BBSRC) for an Industrial CASE studentship
with CABI to R W Rees along with P T P P
London Sumatra Indonesia Tbk (Lonsum).
We wish particularly to thank Hugh Foster
and Steven Nelson for their unfailing support
and advice and for providing the facilities at
Bah Lias Research Station (BLRS), Sumatra.
Also we acknowledge the assistance of the
support staff at BLRS, including Yonnes
Hassan and Oslan Efendi
Thanks to Ursula Potter, Centre for
Electron Optical Studies, University of Bath,
for excellent technical advice with cryo-SEM
and TEM.

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