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 @microbelabThanks to postdoc Xiaohui Gao for her AMAZING talk at the 21st Annual Yale Microbiology Retreat #postdocresearch @YaleMicroPath @microbelab The expanded specificity and physiological role of a widespread N-degron recognin https://t.co/azoSlm8660 https://t.co/zhbosRFV1l10 HOURS AGO

@MicrobeLab Retweeted @AppleCardApple Card gives you 3% Daily Cash on everything you buy from Apple, including your new iPhone. You also get 3% Daily Cash with Uber and Uber Eats when you use Apple Pay. Apply now: https://t.co/kRA7G2xkBB Terms apply. https://t.co/5ZEBEtktgS11 HOURS AGO

@MicrobeLab Retweeted @YaleMicroPathCongratulations to Professor Eduardo Groisman @microbelab, a recipient of the 2019 Yale Postdoctoral Mentoring Award! The prize recognizes faculty who best exemplify the role of a mentor and provide exceptional mentoring to current postdoctoral scholars. #postdocmentor https://t.co/O5Mx6oMYJy4 DAYS AGO

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