Biol. 2320 - Keys to thought questions 3 & 4 Fall 2000
3a.
The point of this question was to think about why keeping the replication
at the continuous and discontinuous strands together in space and time might be
a good thing. The most obvious
answer was that the continuous strand half of the dimer would hold the other
half in the correct position to find the sequence of primers used in the Okazaki
fragments. In other words, the fact
that the continuous strand part of the polymerase holds on and keeps moving into
the replication fork makes it possible for the discontinuous strand part to let
go and then grab o again in the right place.
Another good answer was that coordination of the synthesis of the two
strands would facilitate the orderly termination of a round of replication.
If the two strands were replicating independently, and either one got a
head of the other, there would have to be a mechanisms to stop the one that got
ahead or it could overshoot and start re-replicating a stretch that had already
been done.
Simply re-stating how the system works to facilitate the formation of
Okazaki fragments did not address the question.
Stating that having the strands replicate separately would some how be
more likely to lead to damage or mutation was worth only partial credit unless
you provided a specific example.
3b.
There were 3 correct answers: 1) The heavy/light N DNA incorporated into
the Okazaki fragments was exactly the same as the continuous strand and so would
be the same density, and seen as such by M & S.
2) M & S separated double stranded DNA by centrifugation so the
Okazaki fragments would have moved with the parent DNA and thus not been seen.
3) Okazaki used a different density gradient centrifugation method that
resolved molecules by size as opposed to just density (this information was in
legends of figures 13.3 and 13.10, where it was mentioned that M & S used
CsCl and Okazaki used sucrose as the gradient media respectively).
Stating that M & S used cells in which replication was completed, or
in which the Okazaki fragments were already ligated involved making an
inaccurate assumption. In bacterial cells replication occurs continuously.
Remember the theta structure Dr. Rushing showed where the origin of
replication had “fired” again before the previous round of replication was
complete. Hence there would always
be Okazaki fragments present.
Invoking the difference in labeling of the DNA (that M & S used just density labeling and Okazaki used radioactive labels) missed the point that Okazaki still separated the DNA by density.
4a.
If you chose BER as more similar you would want to argue that BER works
solely on the base that is lesion, and that the glycosylase is like the
photolyase in that it acts directly on the base that is the problem.
If you chose NER you would want to argue that the detection system worked
by identifying a large distortion in the DNA structure (specifically in this
case, the TT dimer).
4b.
If you chose NER as dissimilar you would want to state that there is no
helicase activity, no nuclease activity and no polymerase activity involved in
photoreactivation and all of these are used in NER.
If you chose BER as dissimilar you would want to state that there is no
polymerase activity, that no base is removed, there is no nucelase, no
phosphodiesterase, and no ligase activity.
4c.
The 3 enzymes in common were: DNA endonuclease; DNA polymerase and DNA
ligase. The endonuclease cuts the
DNA once in BER and twice in NER, in both cases to remove DNA to be replaced by
a polymerase. The polymerase replaces the removed region.
The ligase rejoins the gap between new and original DNA.
The helicase is specific to NER. It
unwinds the DNA between the two nicks caused by the endonuclease, causing the
release of the damaged/mispaired base. The
glycosylase and phosphodiesterase are specific to BER.
The glycosylase removes the chemically modified base.
The phosphodiesterase removes the sugar-phosphate component of the
nucleotide that has had its base removed.
4d. Transcribed regions of DNA might be more susceptible to damage because they are constantly being “worked on” by the transcription machinery. DNA binding proteins interact with the bases, distorting normal base-pairing and bending the DNA. RNA polymerase opens up regions of single stranded DNA, which may be unstable. DNA is forced to base-pair with RNA which may lead to chemical changes in the bases.