Encyclopedia of Evolution.pdf - Online Reading Center

found in eukaryotic cells are both the simplified evolutionary
descendants of bacteria.
Bacteria can evolve rapidly. Their populations can
evolve antibiotic resistance within a few years (see resistance,
evolution of). They can also remain the same for
millions of years. Bacteria are very good at evolving, or staying
the same; they are good at metabolizing rapidly, but also
at doing nothing at all. Spores of Bacillus permians from a
250-million-year-old salt deposit near Carlsbad Caverns have
been resuscitated, although scientists are uncertain whether
the bacteria themselves are that old. A type of cyanobacteria
began to grow after spending a century as a dried specimen
in a museum.
Bacteria, while they are as simple as they were three billion
years ago, have contributed enormously to the evolutionary
history of organisms. Humans survive because their cells
are full of the descendants of bacteria.
Further Reading
Dexter-Dyer, Betsey. A Field Guide to Bacteria. Ithaca, N.Y.: Cornell
University Press, 2003.
Stevens T. O., and J. P. McKinley. “Lithoautotrophic microbial ecosystems
in deep basalt aquifers.” Science 270 (1995): 450–454.
Wassenaar, Trudy M. “Virtual Museum of Bacteria.” Available online.
URL: http://www.bacteriamuseum.org/main1.shtml. Accessed March
24, 2005.
balanced polymorphism Balanced polymorphism is the
maintenance of genes in a population because of a balance
between the damage they cause to individuals in homozygous
form and the benefit they confer on carriers. Often, defective
recessive alleles of a gene (see Mendelian genetics) can
cause individuals that carry two copies of the allele (homozygous
individuals) to die. Carriers (heterozygous individuals)
are often unaffected by having one copy of the defective
allele, because they have a dominant allele that functions
normally; the defective allele, in that case, has no effect on
the organism. Because the recessive allele can hide in the heterozygotes,
natural selection may not be able to eliminate
these alleles from populations (see population genetics).
Balanced polymorphism occurs when the heterozygotes are
not only unharmed but actually benefit from the defective
allele.
The most famous example of balanced polymorphism
involves sickle-cell anemia (SCA). The mutation that causes
this genetic disease produces abnormal hemoglobin. Hemoglobin
is the protein that carries oxygen in the red blood
cells. The mutant hemoglobin differs from normal hemoglobin
in only one amino acid, but this difference occurs near
the crucial spot at which oxygen molecules bind. The mutant
form of hemoglobin crystallizes under acidic conditions, such
as during physical exertion, causing the red blood cell to collapse
into a sickle shape. When this occurs, the white blood
cells attack the sickled red cells, forming clumps that tend
to clog the blood vessels. Therefore a person who is homozygous
for the production of the mutant hemoglobin suffers
anemia, first because of the collapse of the red blood cells
into a form that cannot carry oxygen, and second because of
balanced polymorphism
impaired circulation. People with SCA frequently die young.
In a person who is heterozygous for this mutation, half of the
red blood cells have the mutant hemoglobin, therefore the
heterozygous person is mildly anemic. SCA is very common
in tropical regions of Africa and among black Americans
descended from tribes that live in those areas.
People who are homozygous for the normal type of
hemoglobin are susceptible to malaria, which is infection by
a protist (see eukaryotes, evolution of) that lives inside
of red blood cells and is spread by mosquito bites. When, on
a regular cycle, the protists emerge from red blood cells, the
victim experiences fevers and chills. Millions of people die
from malaria. The malaria parasite, however, cannot reproduce
in a red blood cell that contains SCA mutant hemoglobin.
The parasite’s waste products cause the red blood cell to
collapse, and the cell is destroyed, before the parasite has a
chance to reproduce. Therefore, people with SCA cannot also
have malaria. In people who are heterozygous for the mutant
hemoglobin, the parasites can survive in only half of the red
blood cells. This considerably slows the spread of the parasite
and renders the heterozygous person effectively resistant
to malaria. This is an advantage in regions of the world, such
as tropical Africa, that are afflicted with the malaria parasite.
In tropical Africa, therefore, people who are homozygous
for the mutant hemoglobin often die from SCA, people who
are homozygous for the normal hemoglobin often die from
malaria, while heterozygous people survive malaria and pay
for it with mild anemia. The damage caused by the mutant
hemoglobin is balanced by the advantage it provides. A similar
situation explains the prevalence of the blood disorder
thalassemia in some Mediterranean and Asian populations.
Another possible example of balanced polymorphism
involves cystic fibrosis. People who are homozygous for this
mutation have a mutant CTFR protein in their cell membranes.
The mutant protein disrupts salt balance between the
cell and the body. As a result, in people who are homozygous
for the mutation, a buildup of mucus occurs in the respiratory
passages and digestive tract. The mucus buildup encourages
bacterial infections. Certain bacteria that are harmless
to most people, such as Pseudomonas aeruginosa and Burkholderia
cepacia, thrive in the mucus that results from cystic
fibrosis. People who are carriers of the mutant protein have a
slightly greater chance of infection and impaired salt balance,
but not enough to produce noticeable health consequences.
Scientists have puzzled over why the mutation that
causes cystic fibrosis is so common. In some populations,
up to one in 25 people are carriers of this mutation. Salmonella
typhi is the bacterium that causes typhoid fever, a disease
that was common in Europe before the middle of the
20th century. This bacterium binds to the normal form of
the protein. These bacteria cannot bind to the mutant form
of the protein. Therefore, in regions that had typhoid fever,
people homozygous for the mutant protein often died of
cystic fibrosis and people homozygous for the normal protein
often died of typhoid fever, while heterozygous people
were less susceptible to typhoid fever and had only mild salt
balance problems. Today, with the control of typhoid fever
by sanitation and antibiotics, the mutant gene provides no