User:LarryGray:Questions: Difference between revisions
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====Lopes et al==== | ====Lopes et al==== | ||
# What observations lead to the authors' suggestion that discontinuites left randomly behind the fork are not immediately sealed after the passage of the replication fork? | # What observations lead to the authors' suggestion that discontinuites left randomly behind the fork are not immediately sealed after the passage of the replication fork? | ||
Answer: The finding of internal gaps at long distances from the fork with distributions along replicated duplexes that mirrored the length distribution of replicated strands. | |||
====Heller and Marians==== | ====Heller and Marians==== | ||
# How did the author cleverly show that the same DnaB from the lagging strand was involved in leading strand reinitation? | # How did the author cleverly show that the same DnaB from the lagging strand was involved in leading strand reinitation? | ||
Answer: The authors exploited the fact that SSB could exclude further binding of DnaB to Wild-type DnaC. So, the authors pre-loaded DnaB onto the DNA in the absence of SSB then followed up with an SSb incubation that prevented anymore DnaB from loading. This allowed the authors to conclude that leading strand reinitation involved the same DnaB fro mthe lagging strand. | |||
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===Week 3=== | |||
====Moyer et al==== | |||
# According to current understanding, what is the most plausible mechanism for CMG component interaction and how could this be tested? | |||
Answer: Phosphorylation by cdks. Could be tested by site-directed mutagenesis of CMG components to eliminate phosphorylation sites and see if interaction remains. | |||
Latest revision as of 20:23, 24 April 2007
Questions
Week 2
Lopes et al
- What observations lead to the authors' suggestion that discontinuites left randomly behind the fork are not immediately sealed after the passage of the replication fork?
Answer: The finding of internal gaps at long distances from the fork with distributions along replicated duplexes that mirrored the length distribution of replicated strands.
Heller and Marians
- How did the author cleverly show that the same DnaB from the lagging strand was involved in leading strand reinitation?
Answer: The authors exploited the fact that SSB could exclude further binding of DnaB to Wild-type DnaC. So, the authors pre-loaded DnaB onto the DNA in the absence of SSB then followed up with an SSb incubation that prevented anymore DnaB from loading. This allowed the authors to conclude that leading strand reinitation involved the same DnaB fro mthe lagging strand.
Week 3
Moyer et al
- According to current understanding, what is the most plausible mechanism for CMG component interaction and how could this be tested?
Answer: Phosphorylation by cdks. Could be tested by site-directed mutagenesis of CMG components to eliminate phosphorylation sites and see if interaction remains.
