Genetically
 Manipulated 


 

 
 
 Food


 News

1 April 2000

Table of Contents

Financial carrot for GM farmers
potato -all we need to eat
Monsanto to sell NutraSweet for $440 million
baculovirus insecticides
L tryptophan - EMS expert
Should we worry over genetically altered foods?
Eliminating Antibiotic Res Genes
tests for GM crops in fed animals
Biotech Database -- OECD
Bee-t cotton
THE DNA-SEQUENCING BUBBLE
nature biotech apologizes?
Important biotech article posted on web
Virus genes: stinking smut
Bt resistance management
field test of virus
A Cold-Hearted Gene
Isolating the Meningitis Gene: can any good come out of these sequences?

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Date: 26 Mar 2000 15:44:00 U
From: jim@niall7.demon.co.uk

Financial carrot for GM farmers

Saturday, 25 March, 2000, 10:02 GMT

GM crops: Farmers will be paid a tidy sum for trials Farmers who sign up to genetically-modified crop trials could make up to three times as much as they would from growing the equivalent conventional produce.

An investigation by Farmers Weekly found that a farmer who agreed to plant a 10 hectare section of GM oil seed rape would be paid £10,000.

The market value for the non-GM crop would only be £3,700.

Last week Environment Minister Michael Meacher announced there would be more than 60 farm scale trials of GM crops this year.

Despite the generous payments, it seems the government is struggling to get enough farmers to take part in the trials. Only 30 have signed up so far.

Confidentiality clause

BBC environment correspondent Tom Fielden said the government and industry officials are reluctant to talk about the amount of money being paid to farmers because of a confidentiality clause.

However they say the farmer is compensated at the market rate.

Stephen Smith, of the Supply Chain Initiative on Modified Agricultural Crops, (SCIMAC), said farmers will also be paid for the inconvenience and change of management practices.

The SCIMAC is a consortium for the agriculture industry which has supplied the names of willing farmers to the government.

He told the BBC's Radio 4 Today programme: "All new agriculture has to be trialled. Farmers are always paid above and beyond market value because there are many areas in which they are inconvenienced."

He said SCIMAC had given the government more than 100 names of farmers willing to take part although they knew some would back out.

The government has said there is still time for other farmers to be sign up before trials begin next month.

Local opposition

Currently 30 have signed up with another six almost ready.

But two farmers have dropped out citing local opposition as their reason.

Mr Smith called on the hysteria to die down so that farmers can get on with independent trials which would produce hard facts on GM crops.

He added: "This means we can go forward with good science principles and start generating data in which we can make good decisions about the impact of this material."

Seven trials carried out in 1999 proved extremely controversial - two being destroyed by protesters and one by the farmer himself.

Some environmentalists believe that a number of issues surrounding GM crops, such as the risk of cross-pollination of neighbouring crops and contamination of honey - have not been resolved.

Those who object to the tests have vowed to keep up the pressure during the current run of


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Date: 27 Mar 2000 08:12:25 U
From: "j.e. cummins" jcummins@julian.uwo.ca

potato -all we need to eat

Published online before print March 14, 2000 Proc. Natl. Acad. Sci. USA, 10.1073/pnas.050012697

Plant Biology:

Increased nutritive value of transgenic potato by expressing a nonallergenic seed albumin gene from Amaranthus hypochondriacus

By Subhra Chakraborty, Niranjan Chakraborty, and Asis Datta
National Center for Plant Genome Research, Jawaharlal Nehru University
Campus and School of Life Sciences, Jawaharlal Nehru University, New Delhi 110067, India

Communicated by M. S. Swaminathan, Centre for Research on Sustainable Agricultural and Rural Development, Madras, India, January 11, 2000 (received for review September 15, 1998)

Improvement of nutritive value of crop plants, in particular the amino acid composition, has been a major long-term goal of plant breeding programs. Toward this end, we reported earlier the cloning of the seed albumin gene AmA1 from Amaranthus hypochondriacus. The AmA1 protein is nonallergenic in nature and is rich in all essential amino acids, and the composition corresponds well with the World Health Organization standards for optimal human nutrition.

In an attempt to improve the nutritional value of potato, the AmA1 coding sequence was successfully introduced and expressed in tuber-specific and constitutive manner. There was a striking increase in the growth and production of tubers in transgenic populations and also of the total protein content with an increase in most essential amino acids. The expressed protein was localized in the cytoplasm as well as in the vacuole of transgenic tubers. Thus we have been able to use a seed albumin gene with a well-balanced amino acid composition as a donor protein to develop a transgenic crop plant. The results document, in addition to successful nutritional improvement of potato tubers, the feasibility of genetically modifying other crop plants with novel seed protein composition.


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Date: 27 Mar 2000 10:44:47 U
From: jim@niall7.demon.co.uk

Monsanto to sell NutraSweet for $440 million

Reuters Company News - March 27, 2000 09:31
http://www.marketwatch.newsalert.com/bin/story?StoryId=Con7Q0b9Dt....

ST. LOUIS, March 27 (Reuters) – Drug and chemical firm Monsanto Co. said on Monday it agreed to sell its NutraSweet ingredient business, whose products are used in diet sodas and other low calorie sweets, to private equity firm J.W. Childs Equity Partners II LP for $440 million.

Monsanto is also selling its interests in two European sweetener joint ventures – NutraSweet AG and Euro-Aspertame SA – for $67 million in cash to joint venture partner Ajinomoto Co. Inc., Japan's largest seasoning maker.

Monsanto reached these agreements ahead of its pending merger with Pharmacia & Upjohn Inc. that would form a company with $11 billion a year in pharmaceutical sales and $5 billion from genetically modified seeds and agricultural products.

Monsanto agreed in February to sell its NutraSweet tabletop sweetener business, which includes sweeteners for consumer use as opposed to those used by food manufacturers, to an investment group for $570 million.

Monsanto put both sweetener units up for sale last year as part of an effort to reduce billions of dollars in debt it incurred after buying several seed companies in recent years.

The purchases catapulted Monsanto into the No. 2 spot in the U.S. seed market, but also landed the company in the middle of a fierce debate over genetically modified crops.

Supporters of the technology say it reduces the need for herbicides and pesticides by building tolerance in the plants, but critics contend there has not been enough long-term research to conclude the crops are safe for the environment and for human consumption.

Monsanto said that with the sweetener deals plus the $685 million sale of its biogums business, it had completed a restructuring announced in July 1999 that called for selling its consumer and bulk food ingredient businesses.

"We're pleased that the (sweetener) business and its people will have the opportunity to enhance the business in focused, stand-alone entities," Hendrik Verfaillie, Monsanto's president and chief operating officer, said in a statement.

Proceeds from the sale of all of the businesses included in the restructuring plan will be used to pay down debt and for other corporate purposes.

Monsanto has said that once it sold the consumer and food ingredient businesses, it would focus on its agricultural and pharmaceutical units, which make top-selling products including Roundup herbicide and the arthritis drug Celebrex.

Shares of Monsanto closed at 47-1/4 on Friday, off a 52-week high of 50-1/8, up from a low of 32-3/4.


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Date: 27 Mar 2000 18:28:50 U
From: "j.e. cummins" jcummins@julian.uwo.ca

baculovirus insecticides

March 25, 2000 Prof. Joe Cummins e-mail: jcummins@julian.uwo.ca

Genetically Modified (GM) Baculovirus Vectors to Control Insect Pests and for Gene Therapy

Baculovirus are virus that infect insects, they are very stable and may remain dormant in the environment for years before infecting insects. The virus can be purified and produced in quantity to be used in insect control. Since the virus multiplies and persists its use in pest control seems promising. The virus alone has a relatively low killing power and slow action. When a gene for a potent toxin such as scorpion toxin or a gene effecting a juvenile hormone is added to the virus it kills faster and fewer insects survive infection.

Numerous field tests of modified virus sprayed on crops have been undertaken often accompanied by loud expressions of concern from the public. Soon after GM virus were developed for insect control it was found that baculovirus were capable of infecting human liver cells and produced relatively little toxicity to the infected cells. For that reason baculovirus vectors were developed to treat liver disease. Interestingly, the fact that baculovirus can infect human liver cells seems to have been ignored by those developing the virus for commercial pest control.

The following discussion will deal with the use of baculovirus vectors and their safety. I understand that there has been a great deal of pressure to hasten approval of the GM baculovirus for pest control.

Ecological considerations for the impact of recombinant baculovirus insecticides have been studied extensively (Richards et al 1998). The study emphasized baculovirus containing scorpion toxin because that construction has been most widely studied. Impact on non-target insects is extrapolated from insects of related phylogeny, a practice difficult to defend. The recombinant baculovirus were very persistent and capable of reshaping an ecosystem. Modification of baculovirus host range specificity has been achieved by inserting or deleting genes (Theim 1997).

Baculovirus is a circular DNA duplex, it replicates in the insect cell nucleus and replication is prone to the generation of defective genomes by deletion (Wu et al 1999). The mode of virus replication seems to make the recombinant virus highly unpredictable and prone to generating potentially undesirable variants. This important finding has not yet influenced the risk analysis of recombinant baculovirus insecticides and gene therapy vectors.

The scorpion toxins used with recombinant baculovirus have been selected to avoid human neurotoxicity and as much as possible toxicity to non-target animals. However, the allergenicity of toxins and their behavior ( as for example in autoimmunity) in human liver infection has not yet been studied. In insect control the depressant toxin was more effective than the excitatory toxin in recombinant baculovirus (Gershburg et al 1998).

Recombinant baculovirus containing Bacillus thuringiensis toxin have not proven successful in controlling insect pests (Martens et al 1995). However, recombinant baculovirus modifying juvenile hormone proved effective in insect control (Bonning et al 1999). Recombinant baculovirus containing an antisense fragment to the c-myc oncogene proved effective in target insect control (Lee et al 1997). The behavior of the myc oncogene recombinant vector bears careful study regarding non-target animals and its impact during human liver infection.

Baculovirus vectors efficiently transfer genes into human liver cells (Hofmann et al 1995; Boyce and Bucher 1996). The vectors transferred into human liver tissues most effectively in perfused liver tissue because serum components hampered virus transfer (Sandig et al 1996).Human conditions causing defects in complement should allow liver transfer of recombinant baculovirus. Inhibitors of complement facilitate baculovirus gene transfer (Hofmann and Strauss 1998). Hybrid baculovirus-adeno virus vectors have been used to deliver genes to human cells (Palombo et al 1998). Baculovirus vectors have beeen used to deliver hepatitis B to human liver efficiently to allow study of hepatitis B drug therapy (Delaney et al 1999).

In conclusion baculovirus vectors are being used to control insect pests because they are effective and persist for a long time in the environment. Baculovirus vectors are also being used in gene therapy of human liver. These areas of research seem to exist as two solitudes and the risks of one are not evaluated in the context of the other. The most disconcerting finding is the one showing that replication of the baculovirus is inherently unpredictable. However, there may be some who believe that we should all have unlabelled liver gene therapy with our salad.

References

  1. Bonning,B,Possee,R and Hammock,B Insecticidal efficacy of a recombinant baculovirus expressing JHE-KK, a modified juvenile hormone esterase1999 J Invertebr Pathol 73,234-6

  2. Boyce,F and Bucher,N Baculovirus-mediated gene transfer into mammalian cells 1996Proc. Natnl Acad Sci USA 93,2348-52

  3. Delaney,W,Miller,T, and Isom,H Use of the hepatitis B virus recombinant baculovirus-Hep G2 system to study the effects of beta 2',3' dideoxy 3' thiaceydine on replication of hepatitis B virus and accumulation of covalently closed circular DNA1999 Antimicrob Agents Chemother 43,2017-26

  4. Gershburg,E,Stockholm,D,Froy,O,Rashi,S,Gurevitz,M and Chejanovsky,N Baculovirus mediated expression of a scorpion depressant toxin improves the insecicidal efficacy achieved with excitatory toxins 1998 FEBS Lett 422,132-6

  5. Hofmann,C,Sandig,V,Jennings,G,Rudolph, Schlag,P and Strauss,M Efficient gene transfer into human hepatocytes by baculovirus vectors 1995 Proc. Nantl Acad Sci USA 92,10099-103

  6. Hofmann,C and Strauss,M Baculovirus mediated gene therapy in the presence of human serum or blood facilitated by inhibition of the complement system 1998 Gene Ther 5,531-6

  7. Lee,S,Qu,X,Chen,W,Poloumieko,A,MacAfee,N,Morin,B,Lucarotti,C and Krause,M Insecticidal activity of a recombinant baculovirus containing an antisense c-myc fragment 1997 J Gen Virol 78,273-81

  8. Martens,J,Knoester,M,Weijts,F,Groffen,S,Hu,Z,Bosch,D and Vlack,J Characterization of baculovirus insecticides expressing tailored Bacillus thuringiensis Cry1A9b) crystal proteins 1995 J Invertebr Pathol 66,249-57

  9. Palombro,F,Mociotti,A,Recchia,A,Cortese,R,Ciliberto,G and LaMonica,N Site specific integration in mammalian cells mediated by a new hybrid baculovirus-adeno-associated virus vector 1998 J Virol 72,5025-34

  10. Richards,A,Matthews,M and Christain,P Ecological considerations for the environmental impact evaluation of recombinant baculovirus insecticides 1998Ann Rev. Entomol 43,493-517

  11. Sandig,V,Hofmann,C,Steinert,S,Jennings,Gschlagg,P and Strauss,M Gene transfer into hepatocytes and human liver tissue by baculovirus vectors 1996 Human Gene Ther 20,1937-45

  12. Thiem,S Prospects for altering host range for baculovirus bioinsecticides 1997 Curr Opin Biotechnol 8,317-22

  13. Wu,Y and Lui,G and Carstens,E Replication, integration, and packaging of plasmid DNA cotransformation with baculovirus viral DNA 1999 J Virol 73,5473-80

Top PreviousNextFront Page

Date: 28 Mar 2000 03:59:25 U
From: Robert Mann robt_m@talk.co.nz

L tryptophan - EMS expert

This article will be too long for some, and too technical for others. But I make no apology for posting it, as it gives a most expert summary of the difficulties in interpreting the dozens killed and thousands maimed by the GE tryptophan sold by Showa Denko KK.

This disaster is one of the main responses to the "substantial equivalence" crap. This was a single chemical, a natural indeed a required component of our diet, purified better than 99%; yet it caused a nasty epidemic. We cannot be sure that the poisonous impurities were due to the genetic engineering, but the circumstantial evidence is strong.

R

........................

Article published in the National EMS Network Newsletter, Winter 1998

NATIONAL EOSINOPHILIA-MYALGIA SYNDROME NETWORK

MEDICAL ARTICLE


Current Status Of Research On The Eosinophilia-myalgia Syndrome

By Gerald J. Gleich, M.D. http:///www.nemsn.org

It has been almost a decade since the eosinophilia-myalgia syndrome (EMS) epidemic. Readers of this publication know full well the nature of this syndrome with its manifold manifestations and its ability to cause prolonged suffering.

Readers also know the extensive work performed by the state Departments of Health and the Centers for Disease Control showing an association between ingestion of L-tryptophan and the occurrence of EMS and, subsequently, that tryptophan causing EMS was produced by Showa Denko KK. It is noteworthy that both of these associations have come under strong attack.

A summary of these attacks was published in a 1996 supplement to the Journal of Rheumatology (1). The thrust of the critics is that all epidemiological studies of EMS are flawed and, thus, no valid evidence exists that ingestion of L-tryptophan caused the EMS epidemic. Indeed, the very existence of the EMS epidemic is doubted by these critics (2).

Responses to these criticisms have been forthcoming from Kilbourne and his colleagues of the Centers for Disease Control (3) and from Belongia and myself (4). Suffice to say that the criticisms of epidemiological studies of EMS and its relationship to L-tryptophan can be answered point by point and readers interested in this debate should consult references 1-4.

From the perspective of one concerned with discovering the cause(s) of EMS, I must add that patients with EMS symptoms were common in late 1989 and 1990; now, new patients with these symptoms are rare.

Research into the cause of EMS has continued and has focused on contaminants in L-tryptophan implicated in causing EMS. Careful chemical analyses comparing implicated to nonimplicated L-tryptophan have revealed several contaminants, including peak E (1,1'-ethylidenebis[tryptophan]), 3-(phenylamino)alanine and others, including one peak, called AAA, which is especially strongly related to EMS.

These studies show us the chemical contaminants in the L-tryptophan, which are associated with EMS. But association does not prove guilt! What we need is a way to prove that a particular contaminant or a combination of contaminants causes EMS. In one sense, the EMS epidemic was a tragic experiment in which we learned that certain contaminants in Showa Denko L-tryptophan cause disease. But which contaminants and how did they cause disease? Presumably, feeding the contaminants to healthy persons would again cause disease.

But can we identify a surrogate for EMS in patients? Two approaches to this end have been taken: one, to cause disease in an animal fed L-tryptophan, and the other to develop a test tube analysis. Establishment of either an EMS-like disease in an animal fed implicated L-tryptophan (referred to as an animal model) or a response stimulated in a test tube (referred to as a bioassay) would permit identification of the critical contaminants. Dissection of the animal model would permit an understanding of the disease mechanism. It is worthy of emphasis that this approach also applies to the ingredients in the oil causing the Spanish toxic oil syndrome.

Initial results from bioassay experiments with L-tryptophan appeared promising. Results from several laboratories suggested that a bioassay could be established such that cells from patients (and normal persons) could be stimulated by implicated, but not nonimplicated, L-tryptophan. However, more extensive studies have not corroborated these reports and a reproducible bioassay that consistently and robustly discriminates between implicated and nonimplicated L-tryptophan still eludes us (5).

Other studies have tested whether L-tryptophan contaminants are able to stimulate cells, for example, to produce increased collagen, and two studies showed that peak E stimulates human cells to produce collagen (6,7). These results are of interest because increased collagen formation is associated with skin thickening and fibrosis, features characteristic of EMS. However, these findings do not mean that peak E is the cause of EMS; it only establishes that peak E can be associated with an EMS-like characteristic. To date, no bioassay able to consistently and robustly discriminate implicated from nonimplicated L-tryptophan has emerged from research laboratories.

Initial results from animal models of EMS also appeared promising. Two studies in rats showed that skin thickening could be induced by administration of case-associated L-tryptophan or peak E. However, subsequent analyses showed that even nonimplicated tryptophan induced skin thickening (8). In mice, rather comparable results have been shown, and skin inflammation and fibrosis are stimulated by administration of peak E. These assays encouraged hope that an animal model of EMS could be developed. However, additional experiments, summarized by Clauw (9), were not able to reproduce these initial promising results.

Because various strains of mice are available and results could differ strikingly depending upon the strain tested, various strains were analyzed and again none of the animals reproducibly developed EMS-like abnormalities. One contaminant in implicated L-tryptophan is 3-(phenylamino)alanine. This compound is remarkably similar to 3-phenylamino-1,2-propanediol, a substance implicated in the Spanish toxic oil syndrome. The finding of two quite similar molecules from two epidemics with similar manifestations prompted additional studies. In one study, 3-phenylamino-1,2-propanediol (in the toxic oil) was incubated with liver cells and was metabolically transformed into 3-(phenylamino)alanine (the L-tryptophan contaminant) (10).

This finding suggested a common pathway for EMS and toxic oil syndrome with 3-(phenylamino)alanine as a critical molecule. So, an animal feeding study was conducted in which 3-(phenylamino)alanine was fed to mice. Unfortunately, no clear-cut EMS-like picture developed. However, it is possible that the L-tryptophan contaminants are metabolized differently by different species, such that only primates possess the critical cellular machinery to produce the disease. To test this possibility, L-tryptophan was fed to cynomolgus monkeys.

Both case-associated and nonimplicated L-tryptophan were given for 12 weeks; these animals consumed L-tryptophan dosages of 800 mg/kg, which is 10-20 times greater than the dosages consumed by patients who developed EMS. Although the monkeys developed gastrointestinal symptoms (manifested by vomiting), nonetheless no EMS-like abnormalities occurred. Thus, no reproducible animal model of EMS useful for identification of the critical L-tryptophan contaminants and for dissection of the abnormal physiology of EMS has been identified.

The failure of both the bioassay and the animal feeding experiments to yield robust and reproducible results has been a major disappointment. In retrospect, my initial optimism that we could identify a bioassay should have been tempered by recognition of the failure of all attempts to identify bioassays or animal models of the Spanish toxic oil syndrome. The clinical similarities between these two diseases, EMS and the toxic oil syndrome, suggest that they share a common mechanism of disease or pathophysiology.

Failure to identify a means to pursue investigations through a bioassay or an animal model has been disheartening on both sides of the Atlantic Ocean. Thus, one cannot pursue the identification of the individual chemicals causing EMS or the toxic oil syndrome through use of the bioassay nor can one explore the mechanisms by which the disease occurs utilizing the animal model. Thus, the present circumstances regarding EMS (and the toxic oil syndrome) are rather unsatisfactory. In spite of the controversy referred to above, we know that an epidemic occurred. As a consequence of the investigations by the public health authorities, L-tryptophan produced by Showa Denko KK has been implicated as a cause of EMS. Certain contaminants present in the L-tryptophan have been implicated as candidates for causation.

However, we do not know the exact structures and without this knowledge one fears that another epidemic will occur at some time. Recall that the Spanish toxic oil epidemic occurred in the spring of 1981 and the EMS epidemic occurred eight years later. One wonders when the next epidemic of an EMS/toxic oil syndrome-like disease will occur and under what circumstances.

Furthermore, our knowledge of the abnormal physiology of EMS and the toxic oil syndrome is remarkably scant. We know that eosinophilia is stimulated in the blood, but only scant information is available concerning the mechanisms by which this occurs. We know that eosinophil degranulation occurs in tissues, but we do not know whether this causes symptoms or simply is a marker for the disease. Activated lymphocytes of the T lymphocyte variety are present in tissues, but we do not know whether these cells are critical for disease.

The prolonged course of EMS/toxic oil syndrome suggests a continuing stimulus to the body's immune system, but as yet, we have no markers for this and, thus, no ability to define its occurrence or severity. Because the EMS epidemic is now behind us, funding agencies, such as the National Institutes of Health, are not enthusiastic about granting monies for its investigation. One worthy objective of the Network might be to contact your Representatives and Senators in Congress to alert them to the need for investigation of EMS. Our group at Mayo continues to investigate the contaminants in the toxic oil and in implicated L-tryptophan and to pursue animal models and bioassays. Without such tools, further progress in understanding these diseases will depend on the occurrence of another epidemic, an event which no one wants!

(C) Copyright 1998 Gerald J. Gleich, M.D.

Gerald J. Gleich, M.D.
Professor of Immunology and Medicine
George M. Eisenberg Professor of Medicine and Immunology
Departments of Immunology and Medicine
Mayo Clinic and Foundation, Rochester, MN 55905

REFERENCES

  1. Clauw DJ, Pincus T: Eosinophilia-myalgia syndrome: review and reappraisal of clinical, epidemiologic and animal studies symposium. J Rheumatol 1996;23(Suppl 46):1-110.

  2. Daniels SR, Hudson KI, Horwitz RI: Epidemiology of potential association between L-tryptophan ingestion and eosinophilia-myalgia syndrome. J Clin Epidemiol 1995;48:1413-27.

  3. Kilbourne EM, Philen RM, Kamb ML, Falk H: Tryptophan produced by Showa Denko and epidemic eosinophilia-myalgia syndrome. J Rheumatol 1996; 23(Suppl 46):81-8.

  4. Belongia EA, Gleich GJ: The eosinophilia-myalgia syndrome revisited. J Rheumatol 1996;23:1682-85 (Editorial).

  5. Kita H, Mayeno AN, Weyand CM, Goronzy JJ, Weiler DA, Lundy SK, Abrams JS, Gleich GJ: Eosinophil-active cytokine from mononuclear cells cultured with L-tryptophan products: An unexpected consequence of endotoxin contamination. J Allergy Clin Immunol 1995;95:1261-67.

  6. Tagaki H, Ochoa MS, Zhou L, Helfman T, Murata H, Falanga V: Enhanced collagen synthesis and transcription by peak E, a contaminant of L-tryptophan preparations associated with the eosinophilia-myalgia syndrome. J Clin Invest 1995;96:2120-2125.

  7. Zangrilli JG, Mayeno AN, Vining V, Barga J: 1,1-ethylidenebis(L-tryptophan), an impurity in L-tryptophan associated with eosinophilia-myalgia syndrome, stimulates type I collagen gene expression in human fibroblasts in vitro. Biochem Mol Biol Int 1995;37:925-933.

  8. Love LA, Rader JI, Crofford LJ, et al: Pathological and immunological effects of ingesting L-tryptophan and 1,1-ethylidenebis(L-tryptophan) in Lewis rats. J Clin Invest 1993;91:804-811.

  9. Clauw GJ: Animal models of eosinophilia-myalgia syndrome. J Rheumatol 1996;23(Suppl 46):93-8.

  10. Mayeno AN, Benson LM, Naylor S, Colberg-Beers M, Puchalski JT, Gleich GJ: Biotransformation of 3-(Phenylamino)-1,2-propanediol to 3-(Phenylamino)alanine: A chemical link between toxic oil syndrome and eosinophilia-myalgia syndrome. Chem Res Toxicol 1995;8:911-916.
---------------------
Robt Mann, consultant ecologist P O Box 28878 Remuera, Auckland 1005, New Zealand (9) 524 2949
Top PreviousNextFront Page

Date: 28 Mar 2000 08:42:30 U
From: "Nancy Allen" nallen@acadia.net

Judy Foreman is a member of the Globe Staff. Her e-mail address is: foreman@globe.com.

Should we worry over genetically altered foods?

By Judy Foreman, Globe Staff, 3/28/2000, Boston Globe 3/28/00
http://www.boston.com/dailyglobe2/088/science

In the early 1990s, while almost nobody was looking, the biotech industry pulled off quite a coup.

Led by industry giants like Monsanto, DuPont, Novartis and Aventis, genetic engineers began commercializing an idea they'd worked on for years - tinkering with genes to make crops more resistant to insects and herbicides.

The basic idea was clever. If, say, a gene could be inserted into soybean seeds so the plants would be resistant to an herbicide, farmers could spray their fields with that herbicide, killing the weeds without fear that it would harm the cash crop. If a gene could be introduced into corn that would produce a protein toxic to corn-eating caterpillars, farmers could grow that kind of corn without using high quantities of pesticides.

The idea has not only worked - it's worked too well in the eyes of the anti-biotech crowd, which has been staging counter-demonstrations this week in Boston during BIO2000, the biotech industry's annual gig. Yesterday, four protesters were arrested on disorderly conduct charges for dumping 30 soybeans outside the Hynes Convention Center, marring otherwise orderly demonstrations.

Worldwide, the area planted with transgenic crops has soared from 2 million hectares in 1996 to nearly 40 million in 1999, according to the Worldwatch Institute, a research organization based in Washington. In the United States, the world leader in growing genetically modified foods, half of the soybean crop carried the herbicide-resistant gene last year while a third of the corn crop carried the anti-caterpillar gene. or genetically modified, food out of the lab and into the mouths of consumers - who had not been clamoring for it - the biotech industry did not completely answer the one question that consumers care most about: Are GM foods safe to eat?

In theory, they should be. After all, we eat DNA all the time (we just call it steak or fish), so what's an extra gene or two? We eat corn that over the centuries has been cross-bred so many times - the old, Mendelian way - that it bears little resemblance to its wild ancestors.

And, even if a transplanted gene, or a special kind of DNA called a promoter, did have a destructive effect, the damage would likely show up in the plant into which it was inserted, not the humans who ate the plant. Besides, our digestive enzymes should chew up GM food the same way they process everything else we eat.

Among other things, that means that it's unlikely that, say, a gene from a flounder that's inserted into a tomato (as scientists are doing to make tomatoes more resistant to freezing) would somehow lodge itself forever in the human genome. In fact, if it were that easy to transfer genes, scientists wouldn't have to resort to sophisticated tricks to create transgenic animals in the lab: They could just feed them GM food.

Indeed, there's no evidence that any human has ever been harmed by eating GM food. (This is in contrast, by the way, to evidence that some herbal can be harmful.)

Given that 60 percent of the processed food now on the American market contain ingredients that have been genetically engineered (a fact many people don't realize), chances are that if the stuff were dangerous, somebody would have noticed.

But none of this is what really irks consumers - including this one - on both sides of the Atlantic. What is irksome is that, even though GM foods may be safe, there's too little testing to say for sure - and there are no labels to guide us.

We don't know, for instance, whether the proteins made by genes inserted into plants could cause serious, even fatal, allergic reactions. In one notorious case, scientists inserted a Brazil nut gene into soybeans to increase protein. When the hybrid was lab tested in 1996, human antibodies reacted to the nut gene, a sign that the product could have caused allergies in people. Bioengineering could produce novel protein combinations that the human body has never seen before, potentially resulting in serious allergies that said Martin Teitel, executive director of the Council for Responsible Genetics, a Cambridge-based watchdog group.

Another concern is that gene-altered foods may have different nutrient value than standard foods. Though the biotech industry disputes it, GM soybeans may have fewer phytoestrogens than normal, a potentially important change, since some consumers eat soybeans precisely to get the hormone-like effects of these plant estrogens.

Opponents of GM foods also worry that gene-altered crops might contain pesticide residues or, worse in the eyes of some opponents, genes that make pesticides in every cell in the plant. (On the other hand, with some gene-altered crops, farmers can use fewer pesticides than normal.)

And then there's the concern that these crops could increase antibiotic resistance.

Bioengineers use antiobiotic-resistance genes as markers to see whether the genes they put into plants get into the DNA. The worry is that eating the altered food could allow the marker genes to pass into bacteria in the human digestive system, making people resistant to potentially life-saving antibiotics. fumed Val Giddings, a geneticist and vice president for food and agriculture at the Biotechnology Number one, the antibiotic resistance genes used as markers in biotech do not [cause] resistance to antibiotics used to treat human disease. Number two, those resistance genes are already crops improved by biotechology have been subjected to more scrutiny in advance, depth, detail and rigor than any other foods

But have they?

In 1992, faced with the imminent onslaught of GM foods, the FDA decided to regulate those products the same way as new foods created by old-fashioned plant breeding, said Laura Tarantino, deputy director of the office of premarket approval at the FDA's Center for Food Safety and Applied Nutrition.

The agency also decided not to consider genes inserted into foods as which would have required FDA approval before marketing. That there is no requirement that of GM food just because it is

This stance so outraged lawyer Steven Druker, executive director of the Alliance for Bio-Integrity, a nonprofit watchdog group based in Iowa, that he and others filed a lawsuit against the FDA in 1998 seeking mandatory safety testing and labeling of GM foods. That suit is still pending. has grown so intense that some grocery chains are tossing transgenic products off their shelves. That, in turn, is making farmers around the world uneasy about growing gene-altered crops.

Indeed, after four years of rapid growth, farmers are expected to reduce planting of genetically engineered seeds by as much as 25 percent this year, the Worldwatch Institute predicts.

Giddings of the biotech organization counters that, at least in the United States, farmers are increasing their plantings of biotech soybeans. They are planting less GM corn, he conceded, but that's not because of consumer resistance but because that crop, engineered to resist a European corn-borer, is no longer endangered by that pest.

The bottom line is that, even if GM foods are safe, and they seem to be so far, consumers have a right to demand labels so they know what they're eating.

Margaret Mellon, a lawyer, molecular biologist and director of the agriculture and biotechnology program at the Union of Concerned Scientists in Washington, put it this way: deserve the opportunity to know which foods have been altered and to make a choice about whether they want to take any risk at all, even


Top PreviousNextFront Page

Date: 29 Mar 2000 10:39:13 U
From: "j.e. cummins" jcummins@julian.uwo.ca

Eliminating Antibiotic Res Genes

By David Adam, Tuesday 28 March 2000

biotechnology : GM cropped

Imagine a blushing bride cutting her wedding cake and finding a wooden spoon. Or discovering nails in her four-poster wedding bed. The baker's reputation would crumble and the groom would hammer the carpenter. A new technique could now stop biotechnologists leaving behind some of the tools of their trade – antibiotic-resistance genes – in genetically modified (GM) crops.

The spread of antibiotic resistance from GM crops into the environment poses a number of problems. The exact risks are unclear, but even the theoretical chance that such genes could transfer into bacteria makes many people uncomfortable. Now a technique developed by Peter Meyer1 and colleagues at Leeds University, UK, means that antibiotic-resistance genes may never leave the laboratory.

GM crops do not need antibiotic-resistance genes. Like flags that float above lobster pots on the seabed, the genes merely indicate the presence of something more useful. The resistance genes are put into plants in tandem with `effectors': genes conferring benefits, such as pest-resistance or herbicide-tolerance, on the crops.

Not all plant cells receive and accept this DNA package. But exposing modified plants to antibiotics quickly indicates which have, as the others are killed off. All generations descended from survivors then contain both the beneficial gene and the residual antibiotic-resistance `marker' gene.

It does not have to be this way. "It's kind of sloppy and an invitation to criticism to leave antibiotic-resistance genes lying around in plants," says one of the Leeds team, plant biotechnologist Charles Scutt. As the researchers explain in Nature Biotechnology, the link between the two genes can be elegantly severed.

Meyer's group tidies up after itself. Or rather, they encourage the plants to. "Once transgenic material has been selected, the marker gene is dispensable," says Meyer. His team grows GM tobacco (Nicotiana tabacum) plants that neatly snip out these redundant genes from their own genomes.

The technique exploits DNA's strong self-attraction. DNA regularly splits and then recombines with itself at a different place – and certain `homologous' regions, where the sequences are very similar, are more likely to get together.

Meyer's team built a DNA string, or `construct', containing an antibiotic-resistance gene placed between two homologous sections. The antibiotic in question was `kanamycin'. An effector gene was placed outside the homologous bookends.

Constructs spliced into the DNA of tobacco leaf cells give plants the expected resistance to kanamycin, the group finds. Then, a few generations down the line, the marker gene disappears. This happens in just under half of the plants, but some also suffer collateral damage: the effector gene is also deleted.

The technique, "is not always associated with precise homologous recombination," the team admits. But it doesn't need to be. Just one plant with the intended genome reconstruction is enough, and these are fairly easy to pick out.

At present the technique has only been demonstrated with tobacco – a favourite with GM researchers as it readily accepts new DNA. "There is no general reason why this technique shouldn't work with all plant types that GM technology has been applied to, though there could be specific problems with individual species," Scutt says.

This is not the first way of removing antibiotic-resistance marker genes to be developed, but it is the quickest, simplest and most convenient. Previously it could only be done by adding another foreign gene to the plant – to express `helper' proteins that induce DNA deletion – or by cross breeding plants.

Techniques such as these are essential, says Janet Bainbridge, chairperson of the UK's Advisory Committee on Novel Foods and Processes. "Only then can we be 100% certain that there could be no theoretical or actual antibiotic resistance transfer."

1.Peter Mayer Laboratory

© Macmillan Magazines Ltd 2000 - NATURE NEWS SERVICE Nature © Macmillan Publishers Ltd 2000 Reg. No. 785998 England.


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Date: 29 Mar 2000 14:12:40 U
From: "j.e. cummins" jcummins@julian.uwo.ca

tests for GM crops in fed animals

Is there a test to detect meat from animals fed GM corn?

Prof. Joe Cummins, e-mail: jcummins@julian.uwo.ca , 29 March 2000

Rick Charmes' question is a very important one and one that made me think a great deal. I hope others will contribute their points of view. The most significant use of GM corn crops is the final fattening of cattle or other animals) who are being prepared for market. Before or during killing it is easy to test the animal feces for remnants of GM food. Importing countries, for example, may require right to test live animals on the way to export as meat.

Tests for GM crop remnants in meat are not presently available and not perceived by most regulators. A research program is needed to determine whether DNA or protein from GM crops can be detected in the blood of animals fed GM crops. Similar studies would also be useful for humans. There is reason to believe that such tests would yield useful information. The use of DNA, for example, as vaccines shows that the molecule may persist in blood for a long time after injection, breathing or feeding. Research from Professor Dörfler from Cologne (Köln) showed that showed that DNA fragments from animals fed viral DNA were inserted into chromosomes in tissue and even passed the placenta and inserted into chromosomes of the fetus. See below, an experiment on ingested gene transfer to tissues and embryo: Uptake of foreign DNA from the environment: the gastrointestinal tract and the placenta as portals of entry [see comments]
AuthorDörfler W; Schubbert R
AddressInstitut für Genetik, Universität zu Köln, Federal Republic of Germany.
SourceWien Klin Wochenschr, 110(2):40-4 1998 Jan 30
AbstractForeign DNA (deoxyribonucleic acid) is part of our environment. Considerable amounts of foreign DNA of very different origin are ingested daily with food. In a series of experiments we fed the DNA of bacteriophage M13 as test DNA to mice and showed that fragments of this DNA survive the passage through the gastrointestinal (GI) tract in small amounts (1-2%). Food-ingested M13 DNA reaches peripheral white blood cells, the spleen and liver via the intestinal epithelia and cells in the Peyer's patches of the intestinal wall. There is evidence to assume that food-ingested foreign DNA can become covalently linked to mouse-like DNA.
When M13 DNA is fed to pregnant mice the test DNA can be detected in cells in various organs of the fetuses and of newborn animals, but never in all cells of the mouse fetus. It is likely that the M13 DNA is transferred by the transplacental route and not via the germ line. The consequences of foreign DNA uptake for mutagenesis and oncogenesis have not yet been investigated.


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Date: 29 Mar 2000 15:45:17 U
From: "j.e. cummins" jcummins@julian.uwo.ca

Biotech Database – OECD

Biotech Database – OECD http://www.olis.oecd.org/bioprod.nsf

The Organisation for Economic Co-operation and Development (OECD) has launched this prototype database of products derived from biotechnology "to allow regulatory officials in the OECD Member Countries to share information regarding certain products or regulated articles that have been [or will be] approved for commercialization." The database, which is searchable, contains brief information about each (mostly agricultural) "product" (e.g., bacteria, resistant crop strain) and each product's approval process. Database entries are listed by organism (bacteria to oilseed rape) or developing company (AgrEvo to Monsanto). [LXP]


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Date: 29 Mar 2000 18:05:19 U
From: Robert Mann robt_m@talk.co.nz

Bee-t cotton

Steve Sprinkel mentioned

huge acreage in cotton, which, since it is fertilized by bees, is perhaps a more startling issue since the pollen is hoisted off by them and then mingled around with everything else the bees pollinate....with unknown results.

I had not known this plant is bee-pollinated. As an amateur beekeeper, I am concerned to learn it, and I immediately wonder 'where is John Losey, now that we need him?'. Who is researching the significance for bees of the fact that a lot of Bt-cotton has been grown in the USA lately?

For those who don't know this wonderful animal, the honey-bee feeds its larvae largely on pollen. If the Bt toxin is expressed in the pollen of the current GE-Bt-cotton, are bee larvae poisoned to any extent by pollen collected from these GE-plants?

The immediate context is that cotton is an extremely pesticide-sprayed crop in the USA, so we can expect the PR agents to respond - when they feel any call to respond at all - with claims that Bt represents progress. If they make this claim, obvious questions will then be

  1. does Bt-cotton actually get much less pesticide spraying? (Recall the spin 'Monsanto's RR(r) soy needs fewer pesticides' when it turns out that one or two types of pesticide have been obviated but the AMOUNT of pesticide - yes, it's that solid mainstay of Monsanto, Roundup(r) - is several times more than used on ordinary soybean plants.)

  2. what harm has been studied in bee larvae of
    1. 'normal' pesticide-laden cotton
    2. Bt-cotton of various kinds ?
R

----------
Robt Mann, Mulgoon Professor emeritus of Environmental Studies, U of Auckland consultant stirrer & motorcyclist
P O Box 28878, Remuera, Auckland 1005, New Zealand (9) 524 2949


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Date: 30 Mar 2000 01:42:12 U
From: Robert Mann robt_m@talk.co.nz

THE DNA-SEQUENCING BUBBLE

00-1-13 Robt Mann

The enormous venture-capital bubble of DNA sequencing is based on junk science and is grossly overhyped using crude caricatures of biochemistry & genetics.

The recent fad of exaggerating the biological & social significance of genes has been ably criticised by Dorothy Nelkin in her book 'The DNA Mystique', and earlier by Jonathan King one of the pioneer critics of GE and still a prof at MIT. If we really want to improve health & welfare, we know many good methods without gambling on GE; and the outer limit of credible potential benefits from GE is very modest compared with the hype.

To the extent that genes are important, the idea of improving on them by engineering has been overblown.

And the sequencing corporations generally underplay the little-understood importance of the minor bases within DNA. It is not only journalists such as Ms Henig who oversimplify by stating The Big Four Rule OK; your actual 'genome' enthusiast typically tries to patent rows of 3-letter codons in just the 4-letter alphabet of the journos.

But the truth is that other, minor ('odd') bases occur in DNA. Some of them are methylated derivatives of the Big 4, notably Me-C and Me-G; but there are others, and this fact has been known 4 decades. What is actually sequenced is almost always copy molecules made in systems which make not true copies but drongo polymers on the slogan The Big Four Rule OK. Thus the sequences for which patents are sought will be, generally, false.

The leader of the Arabidopsis Genome Project, my sometime MSc student, responds that he thinks odd bases other than Me-C must be very rare, but he admits we 'haven't got a handle on them'.

Even if they were all true sequences, their usefulness is far more limited than the corporations make out. Their general model is: find a mutated sequence correlated with an illness, or failing that a pseudo-illness (e.g. AAT deficiency), and then work up an image of correcting that dud gene either by gene therapy (of which few if any actual examples exist) or by other biochemical intervention. There is more wrong than right with this model.

Along with most other GE, this approach is futuristic rather than realistic. The gene-jockeys, intoxicated with power over life, pretend that they are about to deliver something useful, in order to get funding for their expts from venture-capitalists who don't understand.

-----------------
Robt Mann, consultant ecologist
P O Box 28878 Remuera, Auckland 1005, New Zealand (9) 524 2949


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Date: 30 Mar 2000 10:17:45 U
From: "j.e. cummins" jcummins@julian.uwo.ca

nature biotech apologizes?

The editor of Nature Biotechnology selected some adverse comments for publication of a paper we published elswhere and ignored what we had said. He apologiized? for a clear faux pas. However, the editor seems to be a poor speller ( see my name) and an even worse apologizer. The editor seemed lacking in the area of the precauntionary principle and certainly the area of genetics.

Hazardous CaMV promoter?

To the editor:

In your account (January 2000) of our pre-publication manuscript 1 , you quote the criti-cisms but ignore completely our full rebuttal, which was posted on the web last November 2 . Our manuscript 3 reviews and synthesizes the scientific literature on the 35S promoter of the cauliflower mosaic virus (CaMV), used to give constitutive overexpression of transgenes in practically all GM crops already commer-cialized or undergoing field trials.

The pro-moter functions efficiently in all plants, as well as green algae, yeast, and Escherichia coli. It has a modular structure, with parts common to, and interchangeable with promoters of other plant and animal viruses. It also has a recom-bination hotspot, flanked by multiple motifs involved in recombination, similar to other recombination hotspots including the borders of the Agrobacterium T DNA vector most fre-quently used in making transgenic plants.

The suspected mechanism of recombination– double-stranded DNA break repair–requires little or no DNA sequence homologies, and recombination between viral transgenes and infecting viruses has been demonstrated in the laboratory 4 .

The findings suggest that transgenic con-structs with the CaMV 35S promoter may be structurally unstable and prone to horizontal gene transfer and recombination. The poten-tial hazards are mutagenesis, carcinogenesis, reactivation of dormant viruses, and genera-tion of new viruses. These considerations are especially relevant in the light of recent find-ings that certain transgenic potatoes–con-taining the CaMV 35S promoter–may be unsafe for young rats, and that a significant part of the effects may be due to the construct or the genetic transformation (or both)5 .

Our critics believe the CaMV 35S promoter is not harmful because people have been eating the virus in infected cabbages and cauliflower for many years. What we have been consuming is predominantly intact virus and not naked viral genomes. Naked viral genomes have been found to give full-blown infections in nonhost species that are not susceptible to the intact virus 6,7 .

Moreover, the 35S promoter in the CaMV is a stable, integral part of the virus, and cannot be compared to the 35S promoter in artificial transgenic constructs. Artificial con-structs are well known to be structurally unsta-ble 8 . We know that the 35S promoter in the virus does not transfer into genomes because pararetroviruses, such as CaMV, do not inte-grate into host genomes to complete their life cycle; and viral replication takes place in the cytoplasm 9 . But that says nothing about the 35S promoter in transgenic constructs that are integrated into host genomes.

Proviral sequences are present in all genomes, and have at least one module–the TATA box–in common, if not more; it is not inconceivable that the 35S promoter in trans-genic constructs can reactivate dormant viruses or generate new viruses by recombi-nation. The CaMV 35S promoter has been joined artificially to the cDNAs of a wide range of viral genomes, and infectious virus-es produced in the laboratory 10 . There is also evidence that proviral sequence in the genome can be reactivated 11 .

The fact that plants are loaded with potentially mobile elements can only make things worse. Most, if not all, of the elements will have been tamed in the course of evolu-tion and hence no longer mobile. But integra-tion of transgenic constructs containing the 35S promoter may mobilize the elements. The elements may in turn provide helper functions to destabilize the transgenic DNA, and may also serve as substrates for recombination to gener-ate more exotic invasive elements. In signing on to the International Biosafety Protocol in January, more than 150 governments agreed to implement the precautionary principle.

The available evidence clearly indicates that there are serious potential hazards associated with the use of the CaMV promoter. All GM crops and products containing the CaMV promoter should therefore be withdrawn both from commercial use and from field trials unless and until they can be shown to be safe.

  1. Hodgson, J. Nat. Biotechnol. 18, 13 (2000).

  2. Institute of Science in Society (www.i-sis.org).

  3. Ho, M-W., Ryan, A. & Cummins, J. Microbial ecology in health and disease, in press (2000), and available in electronic form (www.scup.no/mehd/ho).

  4. Wintermantel, W. & Schoelz, J. Virology 223, 156-164 (1996).

  5. Ewen, S.W.B. & Pusztai, A. Lancet 354, 1353-1354 (1999).

  6. See for example, Rekvig, O.P. et al. Sc and. J. Immunol. 36, 487-495 (1992).

  7. Structural instability of artificial vectors is a text-book topic. See Old, R.W. & Primrose, S.B. Principles of gene manipulation, Edn. 5. (Blackwell, Oxford; 1994).

  8. Covey, S. et al. Proc. Natl. Acad. Sci. USA 87, 1633-1637 (1990).

  9. Maiss, E. et al. J. Gen. Virol. 73, 709-713 (1992).

  10. Meyer, M & Dessens, J. J. Gen. Virol. 78, 147-151 (1997).

  11. Nowora, T. et al. Virology 255, 214-220 (1999).

Joe Cummins
Dept. Plant Sciences, University of Western
Ontario, Ontario, Canada

Mae-Wan Ho and Angela Ryan
Department of Biological Sciences
Open University, Walton Hall, Milton Keynes, UK, MK7 6AA

Nature Biotechnology Vol 18 April 2000 ( http://biotech.nature.com )
John Hodgson replies:

An apology is clearly due to Cummings et al. for not having drawn attention in my article to their rebuttal of the critics I cited. In my defense I can only say that my nearly 20 years' experience of science publishing had not pre-pared me to expect a rebuttal to unpublished comments on an unpublished manuscript.

The criticism of my article and their critics is largely misdirected and their choice of sup-porting data (other people's) questionable. They point, for instance, to a range of potential hazards of the structural instability of constructs containing CaMV 35S promoter sequences. Their choice of key published data in support of this proposition is the work of Stanley Ewen and Arpad Pusztai on the intesti-nal effects of potato diets on rats.

Whatever its scientific merits (and those have been widely discussed), that paper does not claim that a significant part of the effects may be due to the construct or the transformation but merely that other parts of the GM construct, or the transformation, could have contributed to the overall effects. In any case, identifying poten-tial hazards is of little use unless the relative magnitude of either the potential or of the haz-ard is described.

Exposure to sunlight after all, even in Milton Keynes or Ontario, will elicit many if not all of the same potential hazards. A more proper comparison, perhaps, would be with the risks from the ingestion of plants pro-duced by conventional breeding (i.e., through random mutagenesis, crossing, and selection).

The other key point made–that naked transgenic DNA containing CaMV 35S sequence might be harmful to humans–is also not well supported by their choice of refer-ence. The work of Rekvig et al. that they cite concerns the inoculation of rabbits with naked BK virus, a human polyomavirus.

How does this evidence of an experimental infection of one mammalian species by an integrating virus from another mammalian species sup-port a thesis that, in essence, seems to be that laboratory-created constructs including pro-moter regions from a plant virus that does not integrate naturally into host genomes will (1) infect humans (2) integrate into human genomes, and (3) cause potential hazards. The final paragraph of Cummings and Ho's letter linking their arguments to the Biosafety Protocol could be considered revealing.

A cynic might posit that the reason their review paper was publicized in December 1999 and January 2000–even though it was not actually published then– was to try to influence decision makers involved in finalizing global rules on the transborder shipment of living modified organisms. However, such a supposition, unsupported as it is by any real data, would require such a convoluted and contorted train of logic as to be utterly unbelievable.

CORRESPONDENCE

Letters may be edited for space and clarity. They should be addressed to:

Correspondence, Nature Biotechnology
345 Park Avenue South, New York, NY 10010-1707, USA
or sent by e-mail to biotech@natureny.com Please include your telephone and fax numbers.
© 2000 Nature America Inc. http://biotech.nature.com


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Date: 30 Mar 2000 14:18:54 U
From: wytze geno@zap.a2000.nl
Posted: 03/30/2000 By mritchie@iatp.org

Great site!
w.

Important biotech article posted on web

Biotech Activists wrote:

Biotech Activists biotech_activists@iatp.org http://www.sustain.org/biotech/library/admin/uploadedfiles/Revivi....

(because of the length of the URL, you will have to cut and paste both lines of it into your browser. You can also find the paper by going to the GE & IPR library http://www.sustain.org/biotech and clicking on "Resources".)

Mark Ritchie, President
Institute for Agriculture and Trade Policy
2105 First Ave. South Minneapolis, Minnesota 55404 USA
612-870-3400 (phone)    612-870-4846 (fax)    cell phone 612-385-7921
mritchie@iatp.org    http://www.iatp.org


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Date: 30 Mar 2000 16:48:03 U
From: "j.e. cummins" jcummins@julian.uwo.ca

Virus genes: stinking smut

The paper below shows an interesting approach. Using virus components is growing ever more popular , the danger is that the virus genes are known to recombine with invading virus and to give rise to virus of great danger.

Nature Biotechnology – Articles

April 2000 Volume 18 Number 4 pp 446 - 449

Antifungal activity of a virally encoded gene in transgenic wheat

Monika Clausen1, Regina Kräuter1, Gabriele Schachermayr2, Ingo Potrykus1 & Christof Sautter1

1. Swiss Federal Institute of Technology Zurich, Universitätstrasse 2, 8092, Zurich, Switzerland
2. Federal Research Station for Agrarecology and Agriculture, Reckenholz 191-201, 8046 Zürich, Switzerland
Correspondence should be addressed to C Sautter. e-mail: christof.sautter@ipw.biol.ethz.ch

The cDNA encoding the antifungal protein KP4 from Ustilago maydis-infecting virus was inserted behind the ubiquitin promoter of maize and genetically transferred to wheat varieties particularly susceptible to stinking smut (Tilletia tritici) disease. The transgene was integrated and inherited over several generations. Of seven transgenic lines, three showed antifungal activity against U. maydis. The antifungal activity correlated with the presence of the KP4 transgene. KP4-transgenic, soil-grown wheat plants exhibit increased endogenous resistance against stinking smut.

Keywords: Triticum aestivum L., antifungal activity, Tilletia tritici, transformation, KP4


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Date: 30 Mar 2000 17:08:17 U
From: "j.e. cummins" jcummins@julian.uwo.ca

Bt resistance management

Bt resistance management [Headlines]

Trends in Plant Science, 2000, 5:4:144
http://www.epa.gov/pesticides/biopesticides

Abstract

There is no abstract for this article. The text below is the first paragraph of text within the article.

The US Environmental Protection Agency (EPA) has announced new measures for resistance management in Bt corn (corn that expresses Bacillus thuringiensis toxins); the industry has agreed to the conditions. The additional measures to fully manage insect resistance this growing season include: a minimum structured refuge of at least 20% non-Bt corn (50% in cotton areas), expansion of monitoring in the field to detect any potential resistance, and for the protection of non-target insects.

It is the first time that resistance management has been introduced before the problem has arisen. The step is seen by environmentalists as an important pro-active step to ensure that these biopesticides can be used effectively for a longer time.


Top PreviousNextFront Page

Date: 30 Mar 2000 18:17:00 U
From: "j.e. cummins" jcummins@julian.uwo.ca

field test of virus

The article below is about the field test of a GM virus related to those infecting human liver in USA. We all fear Gypsy Moth but we should have full dislosure of relevant facts before field tests are allowed. I do not think people shopuld support field tests of virus that may infect human liver.Anybody know about these tests in Mass. USA?

A field release of genetically engineered gypsy moth (Lymantria dispar L.) nuclear polyhedrosis virus (LdNPV).

J Invertebr Pathol 1999 May;73(3):260-8 (ISSN: 0022-2011)

D'Amico V; Elkinton JS; Podgwaite JD; Slavicek JM; McManus ML; Burand JP [Find other articles with these Authors]

Department of Entomology, University of Massachusetts at Amherst, Amherst, Massachusetts 01003, USA. vdamico@erols.com.

The gypsy moth (Lymantria dispar L.) nuclear polyhedrosis virus was genetically engineered for nonpersistence by removal of the gene coding for polyhedrin production and stabilized using a coocclusion process. A beta-galactosidase marker gene was inserted into the genetically engineered virus (LdGEV) so that infected larvae could be tested for its presence using a colorimetric assay. In 1993, LdGEV-infected gypsy moths were released in a forested plot in Massachusetts to test for spread and persistence. A similar forested plot 2 km away served as a control.

For 3 years (1993-1995), gypsy moths were established in the two plots in Massachusetts to serve as test and control populations. Each week, larvae were collected from both plots. These field-collected larvae were reared individually, checked for mortality, and then tested for the presence of beta-galactosidase. Other gypsy moth larvae were confined on LdGEV-contaminated foliage for 1 week and then treated as the field-collected larvae. The LdGEV was sought in bark, litter, and soil samples collected from each plot.

To verify the presence of the LdGEV, polymerase chain reaction, slot blot DNA hybridization, and restriction enzyme analysis were also used on larval samples. Field-collected larvae infected with the engineered virus were recovered in the release plot in 1993, but not in subsequent years; no field-collected larvae from the control plot contained the engineered virus. Larvae confined on LdGEV-contaminated foliage were killed by the virus. No LdGEV was recovered from bark, litter, or soil samples from either of the plots. Copy


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Date: 30 Mar 2000 20:12:08 U
From: Robert Mann robt_m@talk.co.nz

A Cold-Hearted Gene

fw from Wired'(r) "online" daily bull - mainly cybernerdism but some links to GE as you'd expect:

A Cold-Hearted Gene (Technology 3:00 a.m. PST)

http://www.wired.com/news/technology/0,1282,35266,00.html?tw=wn20....

And you thought you just had a cold. – Researchers in Toronto have found the gene that allows one of most common and highly contagious cold viruses to trigger deadly heart disease.

By Kristen Philipkoski.

Speculation for fun & profit: think how much venture capital you could get to fund a GE lab if you glibly touted the vision of commercial

1 vaccines against colds
2 vaccines against heart disease
3 . . . {you fill in other items on the list}

And, to judge by the record so far, as summarised by Nicholas Wade (one of the most experienced USA science journos) in the NY Times, you can expect to pull in bulk venture capital without ever actually selling anything, let alone turning a profit.

That of course still leaves numerous GE labs which conduct potentially dangerous expts. Even if no saleable product emerges, many of those expts could cause widespread ecological harm. Since their containment systems are operated by mainly staff who feel that fears of harm from GE are absurd, it is far too permissive, and it is false, to say "I don't know anyone who is worried about the contained lab expts" as one of our key politicians recently said.

This GE fad is certainly a huge bubble of venture capital pumped up by junk science.

R

--------------
Robt Mann, consultant ecologist, P O Box 28878 Remuera, Auckland 1005, New Zealand (9) 524 2949


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Date: 30 Mar 2000 20:12:36 U
From: Robert Mann robt_m@talk.co.nz

Isolating the Meningitis Gene: can any good come out of these sequences?

http://www.wired.com/news/technology/0,1282,35283,00.html?tw=wn20.... For the second time in a month, researchers decode a gene linked to a

bacterium that causes the disease. The combined information provides new understanding of its most virulent forms.

Collins: Genome Mapped by 2003 (Technology Wednesday)

The head of the public Human Genome Project says the map is two-thirds complete.

----------------------
Robt Mann
Mulgoon Professor emeritus of Environmental Studies, U of Auckland consultant stirrer & motorcyclist
P O Box 28878, Remuera, Auckland 1005, New Zealand (9) 524 2949