Aurelia Battesti
Laboratory of Molecular Biology
8 Papers
Aurelia Battesti is an academic researcher from Laboratory of Molecular Biology. The author has contributed to research in topics: rpoS & Biology. The author has an hindex of 6, co-authored 6 publications.
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Papers
The RpoS-mediated general stress response in Escherichia coli.
TL;DR: The complex transition from exponential growth to stationary phase has been partially dissected by analyzing the induction of RpoS after specific stress treatments, and a better understanding has been led to a better, but still far from complete, understanding of how stresses lead to RPOS induction and what RPoS-dependent genes help the cell deal with the stress.
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Roles of adaptor proteins in regulation of bacterial proteolysis.
Aurelia Battesti,Susan Gottesman +1 more
TL;DR: Advances over the past few years have provided new insight into how adaptor proteins interact with both substrates and proteases and how Adaptor functions are regulated, and an important advance has come with the recognition of the critical roles of anti-adaptor proteins in regulating adaptor availability.
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Stress sigma factor RpoS degradation and translation are sensitive to the state of central metabolism
TL;DR: It is found that a block in central metabolism, via deletion of a gene encoding pyruvate dehydrogenase, leads to a dramatic increase in RpoS in exponential phase cells, allowing reprogramming of E. coli metabolism.
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Anti-adaptors provide multiple modes for regulation of the RssB adaptor protein
Aurelia Battesti,Joel R. Hoskins,Song Tong,Paola Andrea Milanesio,Jessica M. Mann,Andrea N. Kravats,Yodit M. Tsegaye,Alexandre Bougdour,Sue Wickner,Susan Gottesman +9 more
TL;DR: The mutants provide insight into how the anti-adaptors perturb RssB response regulator function and activation and bears similarity to constitutively activated mutants found in a very different PP2C protein.
H-NS Regulation of IraD and IraM Antiadaptors for Control of RpoS Degradation
TL;DR: It is found that H-NS inhibits the expression of iraD and iraM, the genes coding for two antiadaptor proteins that stabilize RpoS when overexpressed, independent from the previously demonstrated regulation by the PhoP/PhoQ two-component system.
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