Need Safeguards for Gene-Tinkered Foods

Wed Jun 23 15:22:22 EST 1993

    I have no objection to anyone participating in a debate on issues
involving transgenic plants, but let's make it open to all and let's
talk about real issues not fantastical, what-if scenarios, the number
and nature of which are limited only by our imaginations.
    Dr. Cummins makes so many claims that are so preposterous that it
is difficult to know where to begin. Moreover, because they are so
devoid of any supporting data and made in such a sensationalist
manner, one has to question whether the author is sincerely
interested in promoting real understanding of the issues. For these
reasons I have avoided commenting on Dr. Cummins numerous claims over
the years in the Canadian press regarding transgenic plants. However,
when I saw this stuff spilling over into Internet and that people
like Haurie Xavier view it as "...detailed explanations..." and
negative comments as "...groundless attacks...", I realized how
persuasive some of this anti-biotech hate literature can become.
    Let's look at just one of Dr. Cummins claims regarding
genetically engineered male sterility for hybrid production
(quoting from the OPIRG message):

    "...What I am saying is that many of the same sterility genes are
likely to affect humans as well as corn, tomatoes and lettuce ..."

    Dr. Cummins does not tell us how this might come about, so we are
left to imagine two possibilities:
    1. the gene products in the plant causing male sterility (RNA,
protein or some other compound) can cause sterility in humans; or,
    2. the gene causing sterility might become part of the human
genetic make-up and cause sterility when it is expressed in the
appropriate tissues.

    The first scenario would be akin to an oral contraceptive and, if
possible, could be regarded as a dramatic breakthrough with
tremendous potential. However, the fact is that we have been eating
hybrid plants (such as tomatoes, carrots, onions and corn) produced
by various male sterility methods for many years. In fact there are
many naturally-occurring mutations in all plant species which cause
male sterility, many of which disrupt meiosis and most of which we
understand very poorly at the molecular level. I predict that, when we
do elucidate the mechanisms of naturally-occurring male sterility,
they will not only include mechanisms that we are using now in
genetically-engineered systems, but will also show us new mechanisms
for accomplishing this.
    The genetic engineering of male sterility in crop plants has been
achieved by methods other than antisense RNA, as mentioned by Dr.
Cummins, but let's look only at this example. An antisense gene is
simply a normal gene (or even portion thereof) which is flipped
around so that it produces a messenger RNA which hybridizes or pairs
with the normal message, thereby disrupting normal expression of the
gene. Or at least that's what is generally thought to happen with
such genes; it is becoming apparent that gene duplications (whether
inverted and/or  truncated or not) might interfere with normal gene
expression in other ways (see Jorgensen, R. 1991. Beyond antisense-
how do transgenes interact with homologous plant genes? Trends
Biotechnol. 9:288). It may even be that a biochemical intermediate
such as RNA is not required for antisense-type approaches to male
sterility to work.
    Even if an unusual  gene product (say, RNA) were produced, what
is the likelihood of that causing male sterility in humans? First
let's consider how much, if any, of that RNA would be ingested. In
most cases, one does not even eat the flower, where the RNA is
produced, but even if one ate the flower portion of a vegetable plant
that was male sterile, how much RNA would be ingested? Since the
antisense gene prevents the development of the male portion of the
flower, there might be only a few cells containing the RNA
originally. How much of that RNA remains after harvest, storage or
cooking (all cells have enzymes that break down RNA)? This is only
the beginning of the fantastic voyage of this RNA. Can it survive in
the gastrointestinal tract long enough to be "picked up" by the cells
lining this tract? Has anyone ever extracted RNA from the contents of
stomachs or intestines (now there's a good project for Joe Cummins)?
How could such RNA, even if it got this far, cross cell membranes to
get into cells of the gi tract? Then, how might this RNA be
transported to the testes? Finally how could this RNA from a plant
gene disrupt spermatogenesis? By hybridization to a similar RNA in
the human cell? Here's where we can be more specific and use the
example of a real plant gene that has been under consideration for
use in male sterility via antisense -  pectate lyase. Pectic
substances are a sort of glue between plant cell walls and this
particular enzyme is thought to be necessary for the separation of
microspores and the formation of pollen. Tell me, Dr cummins, what do
you think the chances are of finding that gene in the human genome
and of it being necessary for the production of sperm?

    The second scenario, that of humans incorporating the gene for
male sterility, adds a new genetic twist to the addage, "You are what
you eat". This scenario can be treated much the same as the one
above, one difference being that in this case the gene is present in
all tissues of the plant. The mechanism of such gene transfer is not
explained by Dr. Cummins, but the outcome of even rare occurrences of
such a process, if possible, should have produced some interesting
looking humans over the many thousands of years that we have been
eating genes from other living things- plants and animals. Aside from
the difficulties of DNA surviving in the gi tract, crossing cell
membranes and becoming stably incorporated in a human chromosome
(another fantastic voyage) of an intestinal cell, how does such a
gene migrate to the reproductive organs, where it becomes active or
is passed on to the next generation? These are only some of the major
hurdles perceived by a plant biologist; talk to someone who really
understands human biology and I'm sure you will find that this
scenario of gene transfer doesn't even make good science fiction.
Finally, once this antisense gene for pectate lyase is transferred to
the human genome, how can it possibly affect spermatogenesis, a
process so radically different from that of producing pollen?

    It is possible to spend hours or days pointing out the numerous,
nonsensical aspects of claims such as these, but you have to ask what
the point is of doing so - the scientists don't need it and the anti-
biotech forces don't want to hear it. I would rather spend time
demonstrating the utility and value of the technology than tilting at

Larry R. Erickson,
Department of Crop Science,
University of Guelph,
Guelph, Ontario,
Canada  N1G 2W1
Fax: 519-763-8933  Phone: 519-824-4120 Ext. 3398

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