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10.03.2026 00:07
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Yes, send me a DM!
Very happy to share some more good news. Our collaboration with Jeffrey Boyd's lab is now published at J Inorganic Biochemistry! Here, Jeff found that iron limitation reprograms S. aureus metabolism towards fermentation. We're grateful to be part of this study.
www.sciencedirect.com/science/arti...
Happy to share that our collaboration with Christina
@stallingslab.bsky.social at WUSTL is out at @pnas.org ! Led by Erin Wang, they found that routing carbon away from peptidoglycans sensitizes Mtb to INH, even in DR-Mtb! Grateful to be part of this project!
www.pnas.org/doi/abs/10.1...
I am recruiting a Ph.D. student in microbial ecology, evolution, and systems biology for fall 2026. Please share!
Details: qevomicrolab.org/Documents/Gr...
Apply by October 1 here: forms.gle/38pPS1Ky84HB...
I'm pleased to share that the preprint for our collaboration study on MIS-C in pediatric COVID-19 patients is now available on medRxiv. In this study led by Marila Gennaro at Rutgers NJMS, we report that antibody repertories vary with clinical presentation of COVID-19 in children.
It's nearing the end of the summer and our undergrads have been presenting on their research at their respective summer research symposia. Terrific work by Jonah Simone at the Rutgers Health BMIHAI Symposium and Gianna Elie at the NJMS URSE Symposium!
I'm excited to share that we've received a NIBIB Trailblazer Award to advance our work on engineering therapeutic macrophages! Grateful for our team and excited to launch this collaboration with the Caleb @bashorlab.bsky.social at Rice!
Thank you @njmicrobe.bsky.social for this really nice writeup about our work!
A study in Nature Communications shows that constitutive hydrolysis of ATP and NADH, or ‘bioenergetic stress,’ potentiates the evolution of antibiotic resistance and persistence in E. coli. #medsky 🧪
@rutgersu.bsky.social published a very nice article about our work!
www.rutgers.edu/news/rutgers...
@njms-mdphd.bsky.social
Many thanks to many members of the Yang Lab who contributed to this project (including many undergrads!) and to our collaborators Douglas McCloskey and Xiaoyang Su! 11/11
@njms-mdphd.bsky.social
We're eager to explore these topics in future projects and to see how generalizable these phenotypes are to pathogenic E coli and other species. We think these mechanisms may inform design of antibiotic adjuvants that can slow or prevent resistance development. 10/n
Importantly, little is known on how energy balance alters bacterial physiology. Although metabolic stress is known to inhibit growth and enhance metabolism, our work is the first to study stress responses and antibiotic phenotypes caused by disrupted energy balance. 9/n
By developing a new assay, Barry showed that mismatches between ATP utilization and production (disrupting ATP homeostasis) are sufficient for augmenting antibiotic killing. Thus, Barry's work introduces new concepts in understanding the interplay between energy balance and antibiotic efficacy. 8/n
Using bacterial genetics approaches, Barry was able to show that bioenergetic stress mechanistically induces stress responses that increase antibiotic stress-induced mutation rates and that protect against antibiotic killing. 7/n
This was also surprising that we previously showed that high levels of reactive oxygen species (ROS) were associated with high antibiotic killing, but the pF1 and pNOX cells had decreased killing while also possessing high levels of ROS! 6/n
Correlations between ATP availability and persistence are known and are usually thought about as correlations between metabolic activity (e.g., dormancy, low ATP) and killing efficacy. But Barry's cells have HIGH metabolic activity, which we previously found to INCREASE antibiotic killing. 5/n
Surprisingly, Barry found that bioenergetically stressed cells evolve antibiotic resistance FASTER than control cells (!!) and are also in general protected from bactericidal antibiotic stress (persistence). 4/n
These strains constitutively hydrolyze ATP (pF1) or NADH (pNOX), creating ATP or NADH sinks in these cells. These in turn induce 'bioenergetic stress' in which the cells are always struggling to meet their energetic demands. 3/n
Barry generated a genetic model system (frequently used by the metabolic engineering community) involving E coli cells over-expressing ATP synthase F1 complex genes (pF1) or heterologously expressing NADH oxidase from Streptococcus (pNOX). 2/n
I'm thrilled to share the newest paper from the Yang Lab! Ever wonder how bacterial metabolism affects antibiotic resistance #AMR? In this study, Barry Li, a former MD/PhD student in the lab, took on this question using a systems and #synthetic_biology approach. 1/n
www.nature.com/articles/s41...
Honored to receive this year's Young Investigator Award from our local ASM branch!
Yang Lab had a terrific time at Rutgers' Biomedical Health Informatics and Artificial Intelligence Symposium yesterday. Great jobs by Yiqi Yan, Oliver Gu, and Reuven Rosen who presented on their work!
Our undergraduate machine learning maestro Edson Petry gave a terrific research presentation this afternoon at the Rutgers Pathways for Junior Scientists Research Program! #Rutgers #NJMS
Would you mind adding me too please? Thanks in advance!
I'm so proud of my technician Lia Goodwin who presented a poster at her first conference at the CSHL Systems Immunology meeting yesterday!
Terrific work by Ethan Bustad, Edson Petry, Oliver Gu, Braden Griebel, and Tige Rustad and wonderful support from our collaborator David Sherman (U Washington)! @rutgershealth.org 6/6
We are now using this work as a launching point for studying how individual (clinical) strains survive host and antibiotic stress and are eager to collaborate if you have some interesting phenotypes that you think are geneically regulated! 5/n
We found that transcription factor activities are better predictors of fitness under hypoxia than TF expression alone. Moreover, these analyses demonstrated that interpretable machine learning can reveal transcriptional programs causally regulating fitness under stress. 4/n
