Regulation of DnaA as a transcription factor by modulation of cooperative binding, and by arrA, an antisense RNA

Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biology, May, 2020

Bibliographic Details
Main Author: Sedivy, Emma L.(Emma Louise)
Other Authors: Alan D. Grossman.
Format: Thesis
Language:eng
Published: Massachusetts Institute of Technology 2020
Subjects:
Online Access:https://hdl.handle.net/1721.1/127137
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author Sedivy, Emma L.(Emma Louise)
author2 Alan D. Grossman.
author_facet Alan D. Grossman.
Sedivy, Emma L.(Emma Louise)
author_sort Sedivy, Emma L.(Emma Louise)
collection MIT
description Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biology, May, 2020
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spelling mit-1721.1/1271372020-09-04T03:21:22Z Regulation of DnaA as a transcription factor by modulation of cooperative binding, and by arrA, an antisense RNA Sedivy, Emma L.(Emma Louise) Alan D. Grossman. Massachusetts Institute of Technology. Department of Biology. Massachusetts Institute of Technology. Department of Biology Biology. Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biology, May, 2020 Cataloged from the official PDF of thesis. Includes bibliographical references (pages 82-96). DnaA is both the bacterial replication initiator and a transcription factor. Both activities are highly conserved and closely regulated. The mechanisms regulating its replication initiation activity have been well studied. Most organisms regulate both the abundance DnaA protein and its activity through a combination of evolutionarily divergent mechanisms. However, the mechanisms governing its role as a transcription factor are poorly understood, especially in Gram-positive organisms like Bacillus subtilis. I described the role of a small antisense RNA in the dnaA region, arrA, which represses dnaA. Mutation of the arrA promoter resulted in increased DnaA levels, which were insufficient to disrupt replication initiation but affected cellular physiology and expression of DnaA targets. In particular, arrA was required for proper sporulation. I also asked whether two of the previously described mechanisms regulating DnaA as the replication initiator in B. subtilis affect its activity as a transcriptional repressor. I found that forms of DnaA that are inhibited for replication initiation are still active transcriptional repressors. This interesting finding raises the possibility that some DnaA targets are regulated in a cell-cycle dependent manner, whereas others are repressed regardless of replication status. by Emma L. Sedivy. Ph. D. Ph.D. Massachusetts Institute of Technology, Department of Biology 2020-09-03T17:48:44Z 2020-09-03T17:48:44Z 2020 2020 Thesis https://hdl.handle.net/1721.1/127137 1191838614 eng MIT theses may be protected by copyright. Please reuse MIT thesis content according to the MIT Libraries Permissions Policy, which is available through the URL provided. http://dspace.mit.edu/handle/1721.1/7582 96 pages application/pdf Massachusetts Institute of Technology
spellingShingle Biology.
Sedivy, Emma L.(Emma Louise)
Regulation of DnaA as a transcription factor by modulation of cooperative binding, and by arrA, an antisense RNA
title Regulation of DnaA as a transcription factor by modulation of cooperative binding, and by arrA, an antisense RNA
title_full Regulation of DnaA as a transcription factor by modulation of cooperative binding, and by arrA, an antisense RNA
title_fullStr Regulation of DnaA as a transcription factor by modulation of cooperative binding, and by arrA, an antisense RNA
title_full_unstemmed Regulation of DnaA as a transcription factor by modulation of cooperative binding, and by arrA, an antisense RNA
title_short Regulation of DnaA as a transcription factor by modulation of cooperative binding, and by arrA, an antisense RNA
title_sort regulation of dnaa as a transcription factor by modulation of cooperative binding and by arra an antisense rna
topic Biology.
url https://hdl.handle.net/1721.1/127137
work_keys_str_mv AT sedivyemmalemmalouise regulationofdnaaasatranscriptionfactorbymodulationofcooperativebindingandbyarraanantisenserna