BMCB625:Discussion Rep Wk2

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BMCB625 Advanced Topics in Molecular Biology


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Lopes et al

  1. 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? Larry's Question Page

Heller and Marians

  1. How did the author cleverly show that the same DnaB from the lagging strand was involved in leading strand reinitation? Larry's Question Page


Lopes et al

  1. If ssDNA breaks are not an artifact of the EM preparation and do indeed occur in vivo, how does DNA damage checkpoint facilitate efficient fork progression?

Heller et al

  1. DnaG (primase) is thought to facilitate replication restart on the leading strand after a stalled fork. What mechanisms does the cell employ to repair these gaps?

Jon's Question Page


  1. In Lopes, et al, why does ablation of TLS activity in rad14 mutants increase the number of internal ssDNA gaps and shorten the distance of internal gaps from the elongation point?
  2. Considering what we know from Heller, et al, how could the in vivo conditions in Lopes, et al be altered to predictably shorten the average observed internal ssDNA gap?

--Chayne 03:10, 11 April 2007 (EDT)



Questions & Answers [[1]]


Lopes et al

Despite the remarkable discovery that DNA polymerase can transcribe through UV lesions when yeast cells lack NER, list potential genotoxic consequences of transcribing through these lesions? [2]

Heller and Marians

Why might the mechanism described by Heller and Marians be considered heretical? [3]