Page 400 - Carrahers_Polymer_Chemistry,_Eighth_Edition
P. 400
Naturally Occurring Polymers—Animals 363
TABLE 10.4
Number of Chromosome of Some Common Species
Organism Chromosome Number * Organism Chromosome Number *
Bacteria 1 Mouse 20
Fruit fl y 4 Rat 21
Pea 7 Rabbit 22
Frog 13 Human 23
Fox 17 Ape 24
Cat 19 Chicken 39
* The diploid chromosome number is double this number except for bacteria.
As noted above one of the important themes is that small, or seemingly small, changes in the
genetic code can have profound effects. Many of the better known diseases contain the names
of the discoveries or unfortunate victim(s). The Wolf–Hirschhorn disease and Huntington’s cho-
rea are such diseases. They are wholly genetically based or in their case, the result of a missing
(Wolf–Hirschhorn) or mutated (Huntington’s) gene. It is believed that the genetic origin of the dis-
ease is contained in chromosome 4. The coding that is responsible for Huntington’s disease is the
sequence CAG. This replication occurs at varying times. If this sequence occurs 35 times or less,
then you will not develop the disease. Counter, if you have this sequence 39 time or more then we
will develop this disease with the onset noticeably beginning in midlife with a slight lose in balance.
There begins a decline in metal capacity, and an onset in the jerking of our limbs. This continues
until death. It generally takes 15–30 years to run its course, but there is currently no cure. In general,
the greater number of repeat sequences, the earlier the onset of the disease. If you have 40 repeat
units, you will exhibit the disease at about 60; if 42 repeat units, you will exhibit the disease by
40; and at 50 you will be well along in the progress of the disease, and most probably dead, by 30.
Thus, the frequency of this sequence in this particular chromosome determines one’s outcome with
respect to this disease. While both diseases are rare, it is the Huntington’s disease that killed noted
folk balladeer Woody Guthrie in 1967.
In the Huntington’s disease, long repeat sequences of CAG appear. The CAG codon codes for
glutamine so that areas that emphasize the buildup of this amino acid appear to offer a greater
incidence of certain neurological diseases possibly whereever they are found. This may be due to
a buildup of glutamine over a time with the glutamine-rich proteins being “sticky” and more apt to
remain at the particular site rather than “moving on” to do what it was supposed to do. After some
time this build up becomes great enough to block the healthy activity of the gene causing problems
and possibly leading to death or noticeable loss of function of the cell. This buildup and death of
a significant number of cells takes time so that is probably why these diseases take time to make
themselves known. As an aside, it is interesting that some health potions emphasize the presence
of glutamine but it must be remembered that while the presence of some glutamine is essential to
healthy lives, it is not the presence of glutamine that may cause these diseases, but rather the coding
on the DNA.
Other repeat sequences appear to also offer problems. Many sequences begin in C and end in G.
Thus, we have large numbers of repeats of CCG and CGG (that code for proline and arginine) that
are believed to give a disposition to certain nerve degeneration related diseases.
Another phenomenon is worth mentioning here. There appears to be a tendency for such repeats
to become longer through each replication cycle. This is called anticipation and is believed to be
related to a very slight tendency for the replication cycle to “lose count” of the number of repeats
as the number of exact repeats becomes large, say 30 or more. Again, this is a reason why some
9/14/2010 3:41:26 PM
K10478.indb 363 9/14/2010 3:41:26 PM
K10478.indb 363

