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Small proteins regulate Salmonella survival inside macrophages by controlling degradation of a magnesium transporter.

The small proteins MgtU and MgtR regulate Salmonella virulence and growth in low Mg²⁺ conditions by controlling the stability of the Mg²⁺ transporters MgtA and MgtB.

FEDS: a Novel Fluorescence-Based High-Throughput Method for Measuring DNA Supercoiling In Vivo.

Map of SupR, a supercoiling reporter plasmid for enterobacteria.

A Physiological Basis for Nonheritable Antibiotic Resistance.The BT4338 regulon in bacteria experiencing carbon limitation.

The three core cellular processes (chromosome replication, transcription, and translation) and coregulatory relationships among them.

A Master Regulator of Bacteroides Thetaiotaomicron Gut Colonization Controls Carbohydrate Utilization and an Alternative Protein Synthesis Factor.

The BT4338 regulon in bacteria experiencing carbon limitation.

Activator of One Protease Transforms Into Inhibitor of Another in Response to Nutritional Signals.

Acetyl-CoA-promoted acetylation of the HspQ protein increases the specificity of the Lon and ClpAP proteases.

The Expanded Specificity and Physiological Role of a Widespread N-degron Recognin.

Candidate ClpS substrates revealed by proteomics.

Salmonella Expresses Foreign Genes During Infection by Degrading Their Silencer.

Salmonella expresses horizontally transferred genes by degrading their silencer, H-NS. HTGs are transcriptionally repressed by H-NS, which binds to their regulatory regions.

Slow Growth Determines Nonheritable Antibiotic Resistance in Salmonella enterica

We report that persistent bacteria form as a result of slow growth alone, despite opposite changes in the abundance of proteins, metabolites, and signaling molecules. Our findings argue that transitory disturbances to core activities, which are often linked to cell growth, promote a persister state regardless of the underlying physiological process responsible for the change in growth.

Dietary sugar silences a colonization factor in a mammalian gut symbiont.

Dietary components are believed to influence the composition of the gut microbiota by serving as nutrients to a subset of microbes, thereby favoring their expansion. However, we now report that dietary fructose and glucose, which are prevalent in the Western diet, specifically silence a protein that is necessary for gut colonization, but not for utilization of these sugars, by the human gut commensal Bacteroides thetaiotaomicron. Our findings underscore a role for dietary sugars that escape absorption by the host intestine and reach the microbiota: regulation of gut colonization by beneficial microbes independently of supplying nutrients to the microbiota.

Sequestration from Protease Adaptor Confers Differential Stability to Protease Substrate.

We report that the Salmonella adaptor ClpS binds to the N terminus of the regulatory protein PhoP, resulting in PhoP degradation by ClpAP. The identified mechanism provides a simple means to spare specific substrates from an adaptor-dependent protease.

Navigating the Gut Buffet: Control of Polysaccharide Utilization in Bacteroides spp.

Metabolic flux controls chondroitin sulfate utilization in Bacteroides thetaiotaomicron.

Protein synthesis controls phosphate homeostasis.

Free cytoplasmic Mg²⁺ inhibits Pi starvation response.

Reduction in adaptor amounts establishes degradation hierarchy among protease substrates.

A reduction in adaptor amounts creates a hierarchy among substrates delivered to a protease by an adaptor. The ClpAP protease degrades certain substrates directly but requires the adaptor ClpS to degrade others.

A protein that controls the onset of a Salmonella virulence program.

Under non‐inducing conditions for the master virulence regulator PhoP (gray), the anti‐virulence protein CigR is expressed independently of PhoP, and the virulence protein MgtC is not expressed (left). At early times under inducing conditions (pink), PhoP promotes expression of MgtC, which, sequestered by CigR, does not inhibit the F1Fo ATP synthase (ATPase) or protect PhoP from degradation (middle). At late times under inducing conditions (blue), MgtC amounts supersede CigR amounts, which result in MgtC binding to and inhibition of the ATPase (right). In addition, MgtC protects PhoP from degradation, thereby increasing PhoP amounts and enabling transcription of a subset of PhoP‐activated genes (right).

When Too Much ATP Is Bad for Protein Synthesis.

Cells' energy and protein synthesis potentials depend on the availability of Mg2+. Bacteria sense and respond to various degrees of Mg2+ limitation. Non-physiological increase in ATP disrupts essential Mg2+-dependent processes. Cell restores free Mg2+ levels by shutting down synthesis of ATP and ribosomes.

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Groisman receives mentorship award

Sugar targets gut microbe linked to lean and healthy people

Nine Faculty Members Appointed to Endowed Positions

In creation of cellular protein factories, less is sometimes more

In creation of cellular protein factories, less is sometimes more