Download Day 58 - upwardsapbio

Finish DNA replication and do a quick overview of Excision Repair. Don’t get too
bogged down with Telomeres, non-coding regions of DNA that play a role in cell
death. When telomeres get short enough…the cell has divided enough, it’s time for
the cell to die.
DNA replication is the process by which DNA untwists and unwinds and a
new DNA strand is created from the parent strand. There are many enzymes and
proteins that aid in this complex process.
After the many enzymes have created this new, semiconservative strand of
DNA, it must then be proofread and repaired. The final, completed strand of DNA
has about 1 in 10 billion nucleotide errors, whereas the differences between the
incoming strand and template strand can be about 1 in 100,000. This shows the
precision of DNA polymerase, which is the enzyme that goes back and proofreads
the DNA strand as it is being made. One method of fixing errors that have
bypassed DNA polymerase is called nucleotide excision repair. In this process,
nuclease cuts out the damaged section of DNA, usually consisting of 2-30
nucleotides, and correct nucleotides are put in the gap by DNA polymerase and
ligase. The chunk that was cut out usually has both correct and incorrect bases.
Some other methods of fixing the DNA molecule include base excision repair,
where only one base is removed, and mismatch repair, where nucleotide bases that
are not correctly paired are fixed.
There is a problem in DNA replication, however, of the lagging strand needing to
me replicated in the 5’ to 3’ direction. To do this, the lagging strand has RNA
primers, which have a 5’ and a 3’ end, put onto a section of the lagging strand, and
DNA polymerase builds more bases from the 3’ end of the RNA
primer.(http://highered.mcgraw-hill.com/olcweb/cgi/pluginpop.cgi?it=swf::535::
535::/sites/dl/free/0072437316/120076/micro04.swf::DNA%20Replication%20For
k) When replication has reached the end of the strand on the lagging strand, a
telomere is extended. A telomere is a repeated extra part of the DNA molecule. In
humans the telomere sequence is TTAGGG. The reason for telomeres is that an
RNA primer is made from the telomere so that the original strand can serve as a
template without the daughter strand being shortened with each DNA replication
process. The enzyme telomerase increases the length of each subsequence telomere
to prevent it from degrading. However, telomerase is not active in most somatic
cells. The normal shortening of telomeres in somatic cells can help regulate how
many DNA replications the cell undergoes, and would presumably lead to the selfdestruction of the cell. (http://highered.mcgraw-hill.com/sites/9834092339/student
_ view0/chapter14/telomerase_function.html) However, in cancerous cells,
research has shown that there is telomerase activity, which can suggest that its
ability to stabilize the telomeres allow the cancer cells to survive and replicate.
1. An uncoded, repeated sequence of DNA that aids in replication of a linear strand is called
what?
a. enzyme
b. telomere
c. chromosome
d. nucleotide
2. Which enzyme provides the initial proofreading of DNA, before excision repair and
mismatch repair occur?
a. amylase
b. ligase
c. DNA polymerase
d. RNA primase
3. True or False: Telomerase is active in most somatic cells of humans.
a. True
b. False
4. Why do cancerous cells continue to replicate uncontrollably?
a. Telomerase is active in these cells, causing them to continue replicating without
shortening telomeres and not self-destruct.
b. They have shorter genetic sequences than normal cells, so they are able to replicate
faster than normal.
c. They do not have an internal clock for how long each phase of mitosis should be, so it
cannot control how fast it replicates.
d. They turn into cannibalistic cells that engulf nearby tissue cells, thus increasing the
size and reproductive ability of the cancer cells.
5. What does nucleotide excision repair cut out to replace with correct nucleotides?
a. The telomere
b. A single nucleotide
c. The whole DNA sequence
d. A small chunk of DNA
1. b
2. c
3. b
4. a
5. d