Agriculture Reference
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which is why human diabetics were able to use insulin extracted from farm animals
to treat their own diabetes. Today, diabetics use insulin produced by microbes genet-
ically engineered to carry and express the human insulin gene. Although microbes
do not ordinarily produce insulin (they have no blood, thus no need for blood sugar
regulation), they are able to read the human origin DNA and from that genetic recipe
make the same protein as is made in humans. This ability shows the universality of
the genetic code, disproving the uniqueness or species proprietary aspect of genes.
Without the commonality of the genetic code across all species, genetic engineering
simply wouldn't work.
This common language of the genetic code, the homology of genes, and synteny in
the order of genes in chromosomes should bury the arrogant concept of proprietary
genes belonging to a given species. The human insulin gene can be read and insulin
synthesized by bacteria. Mice and other mammals carry insulin genes as well, and
they produce insulin sufficiently similar to human insulin as to satisfactorily treat dia-
betics. In humans, the insulin gene recipe is located on the short arm of chromosome
11. In mice, the insulin recipe is located on chromosome 7. And the DNA sequence is
very similar. But this is not unexpected, as mice, unlike bacteria, do have blood and do
need to regulate blood sugar. As the functions are so similar, it's not surprising to find
the DNA base sequence is also similar. But let's take a different approach. Genes are
arranged in a linear fashion along a chromosome, so consider the nearest neighbors
to the human insulin gene on chromosome 11:  on one side, upstream—in the par-
lance of genomics—of the insulin gene in humans is a tumor suppressor gene called
TSPAN 32. On the other side, downstream, is TNNT, a gene for a protein facilitating
fast muscle contraction. These three genes are functionally unrelated, they just hap-
pen to be geographical neighbors. What about our vermin relative? The closest gene
upstream of the mouse insulin gene is TSPAN32. On the other side is—you guessed
it—TNNT. (These genetic comparisons are available online at:  http://www.ncbi.nlm.
nih.gov/IEB/Research/Acembly/. )
At what point is a human gene no longer “human”? If we take the human insulin
gene, for example, and change one or two bases in the DNA, which are so insignifi-
cant that the resulting insulin is identical to the original insulin, is the modified gene
still “human”? Let's go a step further. Let's change a few bases in the DNA, such that
the resulting insulin molecule shows two or three amino acids changed but still fully
functional in regulating blood sugar. Is the modified gene still human or is it syn-
thetic? Finally, what if it turns out that the human insulin gene with a few base changes
is identical to the insulin gene of a musk ox? Have we violated the proprietary genetic
rights of the big beast?
To finally refute the concept of the “species barrier,” consider that transfer of
genetic material from one species to another is actually not unusual in nature.
While fish do not pass their DNA to tomatoes directly, that's due only to physical
barriers, not genetic, as a gene copied from a fish and transferred to a tomato could
settle amid the tomato genome and be treated by the tomato as any other segment of
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