Mycobacterium tuberculosis causes tuberculosis in humans and is one of the leading causes of death by an infectious disease. A signature feature of M. tuberculosis pathogenesis is that the bacterium survives inside macrophages, a host immune cell that kills many other bacteria. The goals of my research program are to: 1) characterize how M. tuberculosis adapts to life inside a macrophage, and 2) apply these discoveries towards the development of new drugs. To achieve these goals we are utilizing genetic, genomic, and biochemical approaches to characterize new genes and proteins that enable M. tuberculosis to succeed as an intracellular pathogen. These findings are then translated into high throughput screening (HTS) platforms to identify small molecule compounds that interfere with M. tuberculosis adaptation physiology. In summary, the mission of my lab is to make basic research discoveries that jump-start the development of new drugs to treat tuberculosis.
Industry Expertise (2)
Areas of Expertise (5)
Cornell University: Ph.D., Plant Pathology
University of British Columbia: B.Sc., Microbiology
MSU nominates undergrad researchers for national Goldwater scholarship
MSU Today online
Werner works as a research assistant in two different labs on campus – under Assistant Professor Robert Abramovitch studying tuberculosis and under Assistant Professor Jubin Cheruvelil studying diabetes among Native Americans and traditional food consumption.
Ancient Chinese malaria remedy fights TB
MSU Today online
In a promising study led by Robert Abramovitch, a Michigan State University microbiologist and TB expert, the ancient remedy artemisinin stopped the ability of TB-causing bacteria, known as Mycobacterium tuberculosis, to become dormant. This stage of the disease often makes the use of antibiotics ineffective.
Simple food additive slows E. coli poisoning
Additional MSU researchers contributing to this study include David Needle and Robert Abramovitch. Alfredo Torres, with the University of Texas, also contributed to this study...
MSU scientists set sights on glaucoma medication to treat TB
MSU Today online
A new discovery by Michigan State University scientists suggests that a common medication used to treat glaucoma could also be used to treat tuberculosis, even the drug-resistant kind. Robert Abramovitch, an MSU microbiologist, along with graduate student Benjamin Johnson who helped lead the study, have discovered that ethoxzolamide, a sulfa-based compound found in many prescription glaucoma drugs, actually turns off the bacterium’s ability to invade the immune system.
Journal Articles (5)
Mycobacterium tuberculosis invasion of macrophages: linking bacterial gene expression to environmental cuesCell Host & Microbe
2007 A central feature of Mycobacterium tuberculosis (Mtb) pathogenesis is the ability of Mtb to survive within macrophages (MØ). Despite its critical importance, our appreciation of the interplay between these two cells remains superficial. We employed microarrays to conduct a stepwise dissection of Mtb-MØ interaction during the invasion of resting bone marrow MØ. Contrary to many bacterial pathogens, engagement by MØ receptors without internalization did not alter Mtb gene expression.
A bacterial E3 ubiquitin ligase targets a host protein kinase to disrupt plant immunityNature
2007 Many bacterial pathogens of plants and animals use a type III secretion system to deliver diverse virulence-associated 'effector' proteins into the host cell 1. The mechanisms by which these effectors act are mostly unknown; however, they often promote disease by suppressing host immunity 2.
Bacterial elicitation and evasion of plant innate immunityNature Reviews Molecular Cell Biology
2006 Recent research on plant responses to bacterial attack has identified extracellular and intracellular host receptors that recognize conserved pathogen-associated molecular patterns and more specialized virulence proteins, respectively. These findings have shed light on our understanding of the molecular mechanisms by which bacteria elicit host defences and how pathogens have evolved to evade or suppress these defences.
A bacterial inhibitor of host programmed cell death defenses is an E3 ubiquitin ligaseScience
2006 The Pseudomonas syringae protein AvrPtoB is translocated into plant cells, where it inhibits immunity-associated programmed cell death (PCD). The structure of a C-terminal domain of AvrPtoB that is essential for anti-PCD activity reveals an unexpected homology to the U-box and RING-finger components of eukaryotic E3 ubiquitin ligases, and we show that AvrPtoB has ubiquitin ligase activity. Mutation of conserved residues involved in the binding of E2 ubiquitin–conjugating enzymes abolishes this activity in vitro, as well as anti-PCD activity in tomato leaves, which dramatically decreases virulence. These results show that Pseudomonas syringae uses a mimic of host E3 ubiquitin ligases to inactivate plant defenses.
Pseudomonas type III effector AvrPtoB induces plant disease susceptibility by inhibition of host programmed cell deathThe EMBO journal
2003 The AvrPtoB type III effector protein is conserved among diverse genera of plant pathogens suggesting it plays an important role in pathogenesis. Here we report that Pseudomonas AvrPtoB acts inside the plant cell to inhibit programmed cell death (PCD) initiated by the Pto and Cf9 disease resistance proteins and, remarkably, the pro‐apoptotic mouse protein Bax.