Research

Our research program seeks answers to a fundamental biological question:
How does an organism know when, where and for long to turn a gene on or off?
We address this question by investigating bacterial species
that establish intimate interactions with animal hosts.
Visit our Research page and Groisman Lab News for more information.

Slow growth determines nonheritable antibiotic resistance in Salmonella enterica. — 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.

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

@MicrobeLab Retweeted @microbelabGroisman Lab mini-reunion at the phage meeting in Madison! Drs. Alexandre Duprey #Supercoiling, Hubert Salvail, Xiaohui Gao, and John May #microbelab #pathogenesis https://t.co/IZ83yBkGvo13 DAYS AGO

@MicrobeLab Retweeted @microbelabCongratulations to former Groisman Lab member Mauricio Pontes, PhD now at Penn State on his new paper in Science Signaling: Slow growth determines nonheritable antibiotic resistance in Salmonella enterica https://t.co/KdVkfUJLtl24 DAYS AGO

@MicrobeLab Retweeted @microbelabCongratulations to former Groisman Lab researcher Jinki Yeom, PhD, on his appointment as Assistant Professor at Duke-NUS Medical School! #basicresearch https://t.co/yMrp9xivUR https://t.co/jwbMHbCe836 MONTHS AGO

Follow @MicrobeLab

Research

Twitter Feed