Science in Society Archive

GM Potatoes not Proven Safe for Release

UK and European regulators authorising release of GM potatoes show reckless disregard of safety. Prof. Joe Cummins

The Sainsbury 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) [1] 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 [2]. The stated aims of the trial are:
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 race.

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 I-SIS [3, 4] (Universal Condemnation Meets UK Government’s Green Light for GM Potato Trials, I-SIS report).

Type of genetic modification of the GM potato

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 resistance genes

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.

Chemical 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 [5]. Recent estimates from the draft potato sequence suggest that the potato contains at least 180 R genes and R gene homologues [1].

The two 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 [6]. 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.

The expression 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 [1]. 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 [1].  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 [7]  and an increased RB transgene copy number produced enhanced transcripts and late blight resistance [8]. 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.

The proposal comments [1] 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, SiS 29).

Field 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 [11] 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.

Article first published 15/07/10


  1. The Sainsbury Laboratory Improving late blight (Phytophthora infestans) resistance in potato using resistance genes from South American potato relatives. APPLICATION FOR CONSENT TO RELEASE A GMO – HIGHER PLANTS

  2. The Sainsbury Laboratory Improving late blight (Phytophthora infestans) resistance in potato using resistance genes from South American potato relative European Commission Institute for Health and Consumer Protection Notification report 2010
  4. Ho MW and Cummins J. Universal condemnation meets UK Government’s green light for GM Potato trials ISIS Report 2006
  5. Foster S, Park T, Pel M, Brignet G, Silwka J, Jagger L, van der Vossen E and Jones J. Rpi-vnt1.1, a Tm-22 homolog from Solanum venturii confers resistance to potato late blight. Molecular Plant-Microbe Interactions  2009, 22, 589–600.
  6. McHale L, Tan X, Koehl P, Michelmore RW. Plant NBS-LRR proteins: adaptable guards.  Genome Biol. 2006, 7(4), 212.
  7. Kramer L.Chouldoir M, Wieigus S, Basskar P, Jiang J. Correlation between transcript abundance of the RB gene and the level of the RB-mediated late blight resistance in potato.  Molecular Plant-Microbe Interactions 2008, 22, 447-55.
  8. Bradeen J Iorizzo M, Mollov D, Raasch J. Colton ?,  Kramer L, Millett B, Austin-Phillips S, Jiang J, Carputo D. Higher copy numbers of the potato RB transgene correspond to enhanced transcript and late blight resistance levels. Molecular Plant-Microbe Interactions 2009, 22, 437-46.
  9. Prescott VE, Campbell PM, Moore A, Mattes J, Rothenberg ME, Foster PS, Higgins TJ and Hogan SP. Transgenic expression of bean alpha-amylase inhibitor in peas results inltered structure and immunogenicity. J Agric Food Chem. 2005, 53(23), 9023-30.
  10. Ho MW. Transgenic pea that made mice ill. Science in Society 29, 28-29, 2006.
  11. Ho MW. GM DNA does jump species. Science in Society 47.

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