FWhy Genetic Engineering Is So Dangerous-By Barry Commoner

Why Genetic Engineering
Is So Dangerous

-By Barry Commoner

Human Genome Project
Background by Barry Commoner
(founder of the Center for the Biology of Natural Systems, Queens
College, CUNY)

The recent reports about the outcome of the Human Genome Project
illuminate the contradictory aspects of molecular genetics and its
application to biotechnology. When the federal effort to create the
Human Genome Project was launched in 1990, the director, James
Watson, defined its purpose as 'The ultimate description of life...that
determines if you have a life as a fly, a carrot, or a man.' This goal
was justified by a singular idea that for decades has dominated
biological and medical research. Enshrined by Francis Crick (with
Watson, co-discoverer of the DNA double helix) as the 'Central Dogma,'
it reduces inheritance, a property that only living things possess, to
molecular dimensions:

Each of a living thing's DNA genes, which collectively comprise the
genome, exclusively governs the formation of each of the individual
proteins that, through their biochemical activity (for example as
enzymes), give rise to the creature's inherited traits. The gene's DNA
carries a 'code' that is represented by the linear sequence of its four
types of components (nucleotides). Through a series of intervening
steps, this code is expected to determine the distinctive linear order
of the amino acids that are strung together to form a particular protein
molecule. Finally, based on this distinctive amino acid sequence, the
protein achieves a specific biochemical activity that gives rise to a
given inherited trait.

In theory, then, by identifying and enumerating all of the human genes
and characterizing the unique sequence of their constituent nucleotides,
the genome project could use the encoded, one-to-one correspondence
between gene and protein to define the molecular structure and therefore
the function of each of the human proteins that determine our inherited

In February, the chief outcome of the genome project was announced. It
was 'unexpected.' After a massive and ingenious search, only about
30,000 human genes were found. Based on the expected one-to-one
gene/protein correspondence, this is too few to account for the 100,000
or more known human proteins. Moreover, by this measure, people are only
about as gene-rich as a mustard-like weed (which has 25,000 genes) and
about twice as genetically endowed as a fruit fly or a primitive worm.
If the human gene count is too low to match the protein count and cannot
explain the vast inherited difference between a weed and a person, there
must be much more to the 'ultimate description of life' than the genes
can tell us. Thus, the main outcome of the genome project was to
contradict the scientific premise on which it was undertaken and to
overthrow, or at least critically damage, its guiding icon, the Central

In retrospect, it is clear that this 'unexpected' result was anticipated
by discoveries made nearly 20 years earlier. In 1982, well before the
genome project was even planned, experiments had shown that protein
enzymes can cut out bits of the DNA that comprises a single gene ('gene
splicing'), which are then reassembled in different ways and prescribe
not just one protein but a variety of them. For example, the several
hundred different proteins that establish the tone-sensitivity of the
array of cells in the cochlea of the inner ear are all derived, by
splicing, from a single gene. Thus, such results contradict the
assumption that a single particular gene exclusively governs the
molecular structure of a single particular protein - and hence the
individual inherited trait that it generates.

This is but one of a series of experimental results that over the last
40 years have contradicted the basic precepts of the Central Dogma.
For example, in the 1960s researchers had already found that the DNA
code is often so poorly copied that it cannot account for the much greater
reliability of biological inheritance itself; here too, it was discovered,
protein enzymes are at work, this time to repair the mis-coded DNA.
Another discordant observation relates to the fact that in order to
become biochemically active and actually generate the inherited trait,
the newly made protein, a strung-out ribbon of a molecule, must be
folded up into a precisely organized ball-like structure. Crick assumed
that the strung-out protein simply 'folds itself up' in the right way. But in
the 1980s, it was discovered that, on their own, nascent proteins are
likely to become misfolded, and therefore remain biochemically inactive -
unless they come in contact with a special type of Achaperone protein
that somehow manages to properly fold them.

Thus, over time experimental evidence has accumulated to show that,
contrary to the Central Dogma, a given gene is not in exclusive control
of an inherited trait. Rather, it exerts its effect on inheritance only
through the intervention of a system of protein-mediated processes, an
arrangement that can give rise to a far more complex array of inherited
traits than can the genes alone.

What has been learned in the last 20 years about the 'prion,' the
infectious agent that causes the Mad Cow disease and related human brain
degenerations is perhaps the most portentous example of the
unacknowledged discrepancies in the Cental Dogma. According to that
theory, biological replication, and therefore infectivity, cannot occur
without nucleic acid. Yet, when scrapie, the earliest known degenerative
diseases of the brain (in sheep), was analyzed biochemically, no nucleic
acid could be found in the infectious material. In 1980, Stanley
Prusiner at the University of California Medical School, San Francisco,
began a detailed study of the infectious agents that cause scrapie and
similar human diseases. His work confirmed that these agents are indeed
nucleic acid-free proteins (which he named prions) and showed that they
replicate in an entirely unprecedented way. Invading the brain, the
prion encounters a normal brain protein, which it then refolds to match
the prion's distinctive three-dimensional structure. The newly refolded
protein itself becomes infectious, and, acting on another molecule of
the normal protein, sets up a chain reaction that propagates the disease
to its fatal end. This process, in which the prion's ability to
replicate is directly transmitted to another protein, contradicts the
Central Dogma, which includes Crick's dictum that the discovery of such
a genetic transfer between proteins '...would shake the whole
intellectual basis of molecular biology.'

All of the foregoing examples are the outcome of research on the
molecular basis of inheritance, typically guided by the precepts of the
Central Dogma. By any reasonable measure, their results contradict the
theory's cardinal maxim: that DNA genes exclusively govern the molecular
processes that give rise to inherited traits. But if nucleic acids are
not solely responsible for inheritance, and if genes do not uniquely
specify protein activity, then it is hazardous to rely on this flawed
theory for assurance that the consequences of genetic engineering are -
as the biotechnology industry claims - entirely predictable. Yet this
conclusion is rarely even mentioned, let alone debated, in the
scientific community. The press has been equally silent on this issue.
For example, a computer search of articles in the major U.S. newspapers
between 1980 and 2000 finds none on chaperones or the infidelity of the
DNA code. That a gene, reassembled from fragments, can govern the
production of a multiplicity of proteins became news only this February
(after it was mentioned in the genome reports), some two decades after
this critical discovery was actually made.

The Central Dogma's ideological grip on the research community has been
so strong that in 1997, when Stanley Prusiner was awarded the Nobel
Prize, several fellow scientists publicly denounced the decision because
his claim that the prion, although infectious, is a nucleic acid-free
protein contradicted the prevailing belief in the Central Dogma and was,
therefore, too 'controversial' to warrant the award. This dogma-induced
bias has seriously impeded not only scientific progress, but human
health as well. In response to the vocal criticism of Prusiner's work,
Ralf Peterson, the deputy chairman of the Nobel Assembly, has pointed
out that, by casting doubt on Prusiner's work (which, incidently,
explained the prion's unique resistance to the conventional
sterilization procedures that were relied on, ineffectually, to control
the disease), his critics delayed effective remedial action against the
Mad Cow disease in Britain for so long that by then it was too late.

How do such discrepancies in its guiding theory affect the reliability
and safety of genetically engineered agricultural crops? This technology
is based on the precept that the specific biochemical properties of a
protein that give rise to a plant's inherited traits are derived, via
the genetic 'code,' exclusively from a particular DNA gene. It follows,
then, that a gene artificially transferred from a wholly unrelated
species - for example, from a bacterium, in which the gene produces an
insecticidal protein - will produce the same outcome, and no more, in a
corn or soybean plant.

Within a single species the overall outcome of the gene's influence on
the protein - and hence on the inherited trait that it governs - is
usually predictable. But this does not reflect the gene's exclusive
control of the inherited trait, since, as we have seen, this outcome
depends as well on an array of other protein-mediated processes such as:
DNA code repair, gene splicing, and chaperone-mediated protein folding.
Rather, the reliability of the natural genetic process results from the
compatibility between the gene system and the equally necessary
protein-mediated systems. This harmonious interaction between the genome
and the protein-mediated systems is developed during their coexistence
over very long evolutionary periods, in which the incompatible variants
that may arise are rejected. In other words, within a single species the
reliability of the successful outcome of the complex molecular process
that gives rise to the inheritance of particular traits is guaranteed by
many thousands of years of testing, in nature, that ensures the
compatibility of its component parts.

In contrast, in a genetically engineered transgenic plant, an alien
bacterial gene must properly interact with the plant's protein-mediated
systems, such as DNA code repair and chaperones. But these plant systems
have an evolutionary history very different from the bacterial gene's.
As a result, in the transgenic plant the harmonious interdependence of
the alien gene and the new host's protein-mediated systems is likely to
be disrupted in unspecified, imprecise and wholly unpredictable ways.
These are revealed by the numerous experimental failures that occur
before a transgenic organism is actually produced and by genetic defects
that occur even when the gene is successfully transferred.

Thus, a recent study has shown that in transgenic bacteria the new
host's code-repair system fails to correct the faulty replication of the
alien gene, a necessary repair process that does occur in the original
host. This means that in the new transgenic host, random uncorrected
errors in gene replication can persist, giving rise to unforeseeable
genetic changes. Similarly, in a recent experiment, a jellyfish gene
that governs the production of a green-glowing protein was successfully
transferred to a monkey egg, and later detected in the tissues of the
resulting offspring. But there, the green glowing protein itself was
absent, signifying a failure in one or more of the processes that must
translate the gene's code into an active protein. Moreover, since the
protein was detected in the egg, this defect arose at some later time,
during fetal development. These are examples of how the disruptive
effect of a 'successful' gene transfer between different species may be
not only unpredictable but also long delayed in its appearance. The
likelihood, in genetically engineered crops, of some instances of even
exceedingly rare, disruptive effects of gene transfer is greatly
amplified by the billions of individual transgenic plants that are
already being grown in the United States.

The degree to which such disruptions do occur in genetically modified
crops is not known at present, for the biotechnology industry is not
required to provide even the most basic information about the actual
composition of the transgenic plants to the regulatory agencies. For
example, in the case of corn plants that carry a bacterial gene for a
specific insecticidal protein, no tests are required to show that the
plant actually produces a protein with the same amino acid sequence as
the original bacterial protein. Yet, this information is the only way to
confirm that the transferred gene is in fact yielding the
theory-predicted product. Moreover, there are no reported studies to
investigate the long-term, multi-generational consequences of the gene
transfer. This would require, for example, detailed analysis of the
molecular structure and biochemical activity of the alien gene's protein
product not only in laboratory test plants, but in the transgenic
commercial crop as well. Since some unexpected effects may appear in
only a fraction of the commercial crop plants, such analyses should be
made in samples grown in different regions that are large enough to
detect plant-to-plant variation in protein products. Given that some
unexpected effects may develop very slowly, crop plants should be
monitored in successive generations as well. None of these essential
tests are being made.

In sum, billions of transgenic plants are now being grown with only the
most rudimentary knowledge about the resulting changes in their
composition. Without detailed, ongoing analyses of the transgenic crops,
there is no way of knowing what hazardous consequences may arise. But,
given the failure of the Central Dogma, there is no assurance that they
will not. The genetically engineered crops now being grown represent a
huge uncontrolled experiment; its outcome is inherently unpredictable.
Our project is designed to help develop effective public understanding
of the dangerous implications of this critical predicament.

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