Death Domains in New Bio-pesticides

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21 Feb 2005 17:36:19 -0000

 

Death Domains in New Bio-pesticides

 

 

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ISIS Press Release 21/02/05

 

Death Domains in New Bio-pesticides

 

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Professor Joe Cummins warns of new bio-pesticides the US

Food and Drug Administration proposes to deregulate that may

cause all animal cells to commit suicide

 

 

 

Programmed cell death universal in multi-cellular organisms

 

Cell death is an important feature of growth and

differentiation in all multi - cellular organisms. In 1972,

the term " apoptosis " was used to describe the cell changes

associated with programmed cell suicide. The death programme

includes blebs appearing on the cell membrane, shrinkage of

the cell, characteristic patterns of DNA fragmentation and

finally disassembly of the cell. Each cell is equipped with

regulatory proteins bearing " death domains " . There is a

common design to the death domains and their regulatory

circuitry in animals and plants. The research on programmed

cell death and anti-death signaling has grown very large and

its implication in cancer care, immunity and even pest

control are being explored. Numerous reviews of the subject

have been written [1-3].

 

The Bacillus thuringiensis (Bt) toxin genes currently

employed in commercial crops are all members of a class of

toxin proteins that accumulate, as crystals, in stationary

stage bacteria (bacteria that have completed their growth

cycle) these genes are designated Cry followed by numbers

and letters that indicate there origin and specificity.

These toxins all create pores in the insect cell membranes

leading to osmotic lysis of the cells, or cells bursting as

they fill up with water.

 

Another kind of Bt toxin, the VIP (vegetative insecticidal

protein) group of toxins are produced in vegetative cells,

the genes are designated VIP followed by numbers and letters

related to their origin and specificity. US Patents

6,291,156 [4] and 6,429,360 [5] from Syngenta Corporation

provided compelling evidence that VIP3A toxin contained

putative death domains and that the toxin induced apoptosis

in insect cells.

 

The " death domain " is a 60 to 70 amino acid long motif,

which is involved in protein to protein interaction, and is

shared by proteins with diverse cellular functions. Some of

the protein members containing death domain motifs include

receptors known to be associated with apoptotic processes,

such as the Fas receptor and the tumour necrosis factor

(TNF) in mammalian cells (references provided in the

patent). The patent admits that, " the death core pathway

seems to be phylogenetically conserved " , while " the signal

transduction pathway from the receptor to the death core

pathway is subject to variation across organisms. "

 

Earlier reports from the United States Department of

Agriculture (USDA) laboratory in Beltsville, Maryland showed

that crude preparations of mixed Bt toxins induced apoptosis

in insect larvae. Agents that induce apoptosis may provide

powerful pest control, but their impacts on non-target

animals and plants need to be carefully evaluated [8] in

view of the evidence that the core pathway is conserved in

evolution while the signal transduction pathway is subject

to variation.

 

A research group from Syngenta published a study showing

that along with apoptosis, VIP3A supported pore formation in

the membrane. The research report noted that the pore

formation mechanism was not mutually exclusive with

apoptosis; but the researchers believed that pore formation

was the main basis for toxicity [9].

 

In 2005, Syngenta petitioned for non-regulated status of

cotton event COT102, a cotton variety resistant to

Lepidopteran pests because it was modified with a synthetic

approximation of the VIP3A(a) gene [10]. The USDA/APHIS

Environmental Assessment of transgenic cotton event COT102

accompanied the petition [11]. Surprisingly both the

petition and the environment assessment appear to have

ignored the aspect of apoptosis and death domains in their

extensive reviews. Even though USDA researchers had

determined that crude Bt toxin preparation induced

apoptosis, the formal reviews and petition appear to have

completely sid e-s tepped the implications of death domains

and apoptosis for non-target animals and plants.

 

The company submission was posted as a docket for public

consultation at http://docket.epa.gov/edkfed/index.jsp

 

04-51-1

 

APHIS-2005-0007 Syngenta Seeds, Inc.; Availability of

Petition and Environmental Assessment for Determination of

Nonregulated Status for Cotton Genetically Engineered for

Insect Resistance 01- 28-2005 General Docket Notice 03-29

 

04-51-2

 

Syngenta Petition 03-155-01p for Determination of

Nonregulated Status for Lepidopteran Resistant Event COT102

 

Comments have to be submitted prior to the closing date, 29

March 2005. The main question is: " have adequate safety

tests been done to allow exposure to the toxin and its gene

in fiber, food and feed? "

 

It is not at all clear that the studies have been adequate.

 

References

 

Bhardwa A. and Aggarwa B. Receptor-mediated choreography of

life and death Journal of Clinical immunology 2003, 23, 317-

32.

 

Nam J, Mani K, Ashton A, Peng C, Krishnamurthy B, Hayakawa

Y, Lee P, Korsmeyer S and Kitsis R. Inhibition of both the

extrinsic and intrinsic death pathways through nonhomotypic

death-fold interaction Molecular Cell 2004, 15,901-12.

 

Barnhart B, Lee J, Alappat E.and Peter M. The death effector

domain protein family Oncogene 2003, 22, 8634-44

 

Estruch J. and Yu C. Plant Pest Control 2001 US Patent

6,291,156.

 

Estruch J, Warren G, Desai N, Kozeil M, and Nye G. Plant

Pest Control.2001 US Patent 6,429,360.

 

Loeb M, Martin P, Narang, N, Hakim, R, Goto S. and Takeda,

M. Control of life, death, and differentiation in cultured

midgut cells of the lepidopteran, Heliothis virescens . In

Vitro Cell Dev Biol Anim . 2001, 37,348-52

 

Loeb M, Hakim R, Martin P,Narang N, Goto S and Takeda M.

Apoptosis in cultured midgut cells from Heliothis virescens

larvae exposed to various conditions. Archives of Insect

Biochemistry and Physiology 2000, 45:12–23.#

 

Cummins J. New GM toxin looms over our food 2003

http://www.i-sis.org.uk/full/NGMTLOOFFull.php ISIS Press

Release 02/12/03

 

Lee M, Walters F, Hart H, Palekar N and Chen J. The mode of

action of the Bacillus thuringiensis vegetative insecticidal

protein Vip3A differs from that of Cry1Ab endotoxin. Applied

and Environmental Microbiology 2003, 69,4648-57.

 

Artim L. Application for determination of non- regulated

status for lepidopteran insect protected VIP3A cotton

transformation event COT102 2005

http://www.aphis.usda.gov/brs/aphisdocs/03_15501p. pdf

 

USDA/APHIS Environment Assessment Syngenta Petition 03-155-

01p for determination of noinregulated status for

lepidopteran resistant event COT102 2005

http://www.aphis.usda.gov/brs/aphisdocs/03_15501p.pdf

 

 

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