ISIS Report 15/07/10
GM Potatoes not Proven Safe for Release
European regulators authorising release of GM potatoes show reckless disregard
of safety Prof. Joe Cummins
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Laboratory John Innes Centre has begun open field tests on genetically modified
(GM) potatoes made resistant to late blight (Phytophthora infestans)
using resistance genes from South American potato relatives. Permission for a
three year field release study ending 30 November 2012 was granted by UK Department
for Environment Food and Rural Affairs (DEFRA)  and by the European
Commission Institute for Health and Consumer Protection. The trial site is not
to exceed 300 sq m per year and should include no more than 400 plants per year
. The stated aims of the trial are:
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1. To demonstrate that the transferred resistance genes offer a valuable method
for controlling late
blight of potatoes which does not rely on agricultural inputs (pesticides).
2. To confirm that the
transferred resistance genes still function in a ‘real life’ situation (i.e. in
a field as opposed to a lab/greenhouse).
3. To expose plants containing the newly identified genes to the local
populations of late blight to confirm that they are indeed useful.
4. If infection does result in disease, to isolate the corresponding pathogen
The GM potatoes
in the current release contain genes from South America potatoes that are
unique members of a group of potato blight resistant genes, other members of
which were in BASF’s GM blight resist potatoes field tested near Cambridge in
2007 and 2008, and criticised by ISIS [3, 4] (Universal Condemnation Meets
UK Government’s Green Light for GM Potato Trials, ISIS report).
Type of genetic modification of the GM
The GM potatoes contained DNA sequences from
two bacterial plasmids, each containing a resistance
gene that targets different strains of P. infestans. Plasmid pSLJ21152
contains resistance gene Rpi-vnt1.1 originating from the wild South
American potato relative Solanum venturii under the control of its
native promoter and terminator regions. Plasmid pSLJ21153 contains resistance
gene Rpi-mcq1.1 originating from the wild South American potato relative
Solanum mochiquense, also under the control of its native promoter and
terminator regions. Plasmid pSLJ21153 contains in addition a truncated copy of
a resistance with moderate (77 percent) identity to the Rpi-mcq1.1 gene
and is believed to be non-functional because it seems to lack a promoter. The Rpi-vnt1.1.
gene insert was accompanied by a nptII gene from E. coli for kanamycin
resistance under the control of a promoter and terminator from nopaline
synthase gene from A. tumefaciens. The Rpi-mcq1.1. insert was
accompanied by a nptII gene under the control of a CaMV (cauliflower mosaic
virus) 35S promoter ocs 3’ (octopine synthase) terminator from A.
tumefaciens [1, 2].
The parasite and
Late potato blight is one of the most
devastating plant diseases caused by the fungus, Phytophora infestans, a
pathogen of the potato and, to a lesser degree, the tomato. In the potato, Solanum
tuberosum, there are four main dominant genes for resistance to blight
infection, R1 through R4. An additional seven genes were identified, five of
which are alleles of the complex R3 locus (for a total of 11 dominant R genes).
Hybridization with wild Mexican species began in 1909 and continues to the
present. However, in spite of constant effort, the P. infestans fungus
rapidly developed strains that overcame the genetic resistance.
fungicides have been developed to control blight but these also succumbed to
the versatility of the fungus. The fungus has two mating
types (fungal mating types are the sexes of the fungus, the gene products of
the mating types allow the two types to fuse then form diploid nuclei that
undergo meiosis leading to gene exchange to form progeny with multiple
genotypes. P. infestans fungus has
mating types (A1 and A2), both of which appeared first in Mexico. Only the A1 mating type was present in European potatoes
until 1978 when the A2 mating type appeared in Britain, prior to that date the British fungus had no sex life. The presence of the two
mating types greatly enhances gene exchange leading to accelerated loss of
genetic resistance and fungicide control [3, 4].
Two main types of resistance to
late blight have been described in potato are field resistance and (R) gene-mediated
resistance. Field resistance (also referred to as quantitative
resistance) is frequently attributed to major quantitative trait loci (QTL)
and a few minor QTL . Field resistance is considered to be more durable than
resistance conferred by single R genes. However, partial resistance (the effect
produced by a single gene member of a quantitative trait) is also strongly
correlated with maturity type (partial résistance to P. infestans
always coincides with late foliage maturity) and, thus, makes resistance breeding
more difficult . Also, the genetic positions of QTL often correspond to
regions of R gene clusters Specific resistance is based on major dominant R
genes. In early breeding programmes during the first
half of the twentieth century, 11 R genes (R1 to R11) were identified in S.
demissum, a wild species originating from Mexico. The S.demissum
genes R1, R3, and R10 have been heavily relied on for blight resistance in
major breeding programs within Europe. As a result, the R genes introgressed
from S. demissum to cultivated potato lines have been overcome as new
pathogen strains evolve that are virulent on the previously resistant hosts.
This ability of P.infestans to rapidly overcome R genes limits the durability
of any single R gene. Although some of the S. demissum genes such as
R5, R8, and R9 have not been used in European cultivars, isolates of P.
infestans that overcome these genes are known. However, it is possible that
by deploying multiple R genes in an otherwise genetically uniform crop, the
ability of P. infestans to overcome these genes may be impaired . Recent
estimates from the draft potato sequence suggest that the potato contains at
least 180 R genes and R gene homologues .
potato R genes in the John Innes GM potato on trial are dominant in expression,
and members of a large family of plant pest resistance genes called nucleotide-binding
site leucine-rich repeat (NBS-LRR); the two R genes belong to the subfamily
‘coiled coil’ (CC-NBS-LRR). NBS-LRR genes code for proteins that monitor the
status of other proteins targeted by the pathogen . These genes are similar
in sequence to mammalian genes involved in regulating the innate immune system.
Problems with the open field trial
The Sainsbury field
release proposal raises several concerns; one is the low level at which the
inserted genes are expressed. The proposal comments: “Given the low levels of
expression observed, we expect that the inserted genes are present as 1-2
copies.” Surely, the insert copy number should have been determined before the
GM potatoes are released to the environment.
of the resistance genes Rpi-vnt1.1 and Rpi-mcq1.1 in the transgenic plants to
be released is governed by their respective native promoters and terminators. R
genes of the same class (NB-LRR) have previously been shown to exhibit very weak
activity . Consequently, the low expression of the transgenes is not surprising.
Despite the very low expression level, the transgenic
plants are reported to be resistant to strains of P. infestans that are
able to cause disease on control, non-transgenic plants . As a rule, it is
highly unwise to expose a microbial pathogen to low level of any control agent
whether it is a chemical or a biological agent. Such low levels promote the selection
of resistant pathogen mutants. A CC-NBS-LRR gene called RB from S.
bulbolbocastanum was found to have a correlation between gene transcript
abundance and the level of late blight resistance in
the potato  and an increased RB transgene copy number produced enhanced
transcripts and late blight resistance . The low CC-NBS-LRR transcription
activity in the potatoes of the Sainsbury release may
promote the evolution of further late blight resistance in the field.
proposal comments  that the potato plants are not expected to exert any toxic, allergenic or other harmful effects on
human health because the introduced genes are members of a class of resistance
genes “already known to be abundant within potato and other plant genomes” and
are members of a particular class of R genes that contains the majority of plant R genes identified thus far, and “each
possesses the same protein structure.” The comment cannot be must be right because
there must be differences in the structure of the R gene proteins to protect
against different pathogens. Furthermore, as the transgenes were obtained from different
species - Solanum venturii and Solanum mochiquense – the
transgene protein products may well be different from the native, non-transgene
equivalents. It should be recalled that the transfer of genes between closely related
species may actually lead to proteins with powerful (sometimes fatal) immune
responses [9, 10] (Transgenic Pea that Made Mice Ill,
testing of broad spectrum NBS-LRR genes has begun with the potato blight
resistant strains. Broad spectrum pest resistant strains of rice, maize,
soybean, and numerous food crops will soon follow. It is imperative that the
safety of these genetic modifications to humans and the environment be fully
evaluated before the GM crops are commercialized.
In addition, the safety of the kanamycin
resistance gene is strongly contested (see  GM
DNA Does Jump Species, SiS 47).
Safety assessment of the GM potato has been notably
inadequate and the approved release shows a reckless disregard of safety and is
in breach of the precautionary principle.