Yi Xing Ph.D. [Former faculty]

Chad E Grueter Ph.D.

Current
Chad
E
Grueter
Ph.D.
Associate Professor
Internal Medicine
Research area(s): 
Regulation of Gene Expression in Development and Disease
Address
Research
Research Focus: 

Our laboratory studies transcriptional processes that are disrupted in disease. We identified a novel transcriptional signaling pathway in the heart that mediates the heart’s ability to regulate whole body metabolism. Through a combination of pharmacological and genetic gain- and loss-of-function studies in mice, we found the heart is capable of regulating whole body metabolism through a mechanism that is governed by MED13 and miR-208a. MED13 is a particularly interesting component of the Mediator complex because it functions as a molecular bridge between the core complex and kinase submodule, providing a mechanism for spatial and temporal control of Mediator-dependent regulation of transcription. In addition, we are studying the function of multiple components of Mediator including CDK8, CDK19, MED12 and CycC. We primarily utilize mutant mouse models to study the proteomic, molecular, bioinformatic and biochemical methods to study the molecular signaling events controlling cardiac response to stress.

Ferhaan Ahmad M.D., Ph.D.

Current
Ferhaan
Ahmad
M.D., Ph.D.
Associate Professor of Internal Medicine and Radiology
Department of Internal Medicine, Division of Cardiovascular Medicine
Address
1191D
ML
1191
ML
Research
Research Focus: 

Dr. Ahmad is the Director of the Cardiovascular Genetics Program at the University of Iowa, which brings together basic scientists at the Carver College of Medicine and clinicians at the University of Iowa Hospitals and Clinics (UIHC) who are focusing on heritable cardiovascular disorders. He directs a laboratory conducting basic and translational research into the genetic and genomic mechanisms underlying inherited cardiovascular disorders, including hypertrophic cardiomyopathy, dilated cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, glycogen storage cardiomyopathy, inherited arrhythmias, and pulmonary hypertension. His laboratory uses laboratory uses a wide range of techniques in human and mouse genetics and genomics, and fosters crosstalk between clinical studies, human molecular genetic studies, animal modeling, basic cellular and molecular studies, and computational systems biology analyses. At the UIHC Cardiovascular Genetics Clinic, an interdisciplinary team evaluates, counsels, and treats patients with inherited cardiovascular disorders and their families.

Veena Prahlad Ph.D.

Current
Veena
Prahlad
Ph.D.
Associate Professor
Biology
Research area(s): 
Neuronal control of cellular stress responses
Address
338
BBE
331
BBE
Research
Research Focus: 

Cellular protein misfolding leads to the occurrence of amyloid oligomers and protein aggregates inside the cell.  Protein misfolding is the cause of cellular dysfunction associated with numerous diseases such as cardiomyopthy, Huntington’s disease, Alzheimer’s disease, adult onset diabetes, cancer and others.  To protect themselves against toxic stressors and concomitant protein aggregation, all cells possess highly conserved surveillance and repair mechanisms. One of the most central of these is the stress responsive transcriptional program called the ‘heat shock response’, controlled by the heat shock transcription factor 1 (HSF1). HSF1 upregulates a set of cytoprotective proteins, the so-called heat shock proteins (HSPs) which help refold and/or degrade damaged proteins to restore homeostasis.  Previously, we have shown that in the animal model Caenorhabditis elegans the upregulation of HSPs upon protein misfolding is not regulated cell autonomously by the amounts of protein misfolding, but instead, is under the control of the organism’s nervous system.  Our lab works on understanding how the nervous system of C. elegans controls the cellular response to stress and protein misfolding. Specifically, we use the powerful genetic techniques afforded to us by the use of C. elegans to ask:

a)  What genes and signaling pathways are involved in how the nervous system detects suboptimal environmental conditions, or stress
b)  What signaling pathways are responsible for transmitting this information to non-neuronal cells
c)  How is the accumulation of protein damage in non-neuronal cells communicated to the nervous system
d)  How do these signaling mechanisms ultimately result in an adaptive, organimal response to macromolecular damage and stress.

Albert J Erives PhD

Current
Albert
J
Erives
PhD
Associate Professor
Biology
Research area(s): 
Bioinformatics, Developmental Genetics, Evolutionary Genetics, Gene Expression and Regulation
Address
424A
BB
424
BB
Research
Research Focus: 

The Genetics of Eukaryotic Transcriptional Enhancers

Transcriptional enhancers are DNA sequences that specify inducible, spatiotemporal patterns of gene expression at most gene loci. Several complementary results from genomic studies have shown that the majority of functional sites in a genome correspond to transcriptional enhancer sequences, thus underscoring their importance for understanding basic physiology. However, while transcriptional enhancers represent a major class of regulatory DNAs in eukaryotic genomes, the entire set of sequences that are necessary and sufficient for constructing a complex eukaryotic enhancer are not yet known.

Our laboratory is focused on using molecular biology, genomics, bioinformatics, and transgenic model systems to understand enhancer biology. A major area of focus in our laboratory is the study of how different morphogen-concentration specific responses are encoded at different loci. We are also interested in understanding the sequence-function relationship well enough to understand the complex patterns of molecular evolution occurring at enhancer sequences.

M. Bento Soares PhD

Professor
Pediatrics

Dana Levasseur Ph.D.

Assistant Professor
Internal Medicine

Craig D Ellermeier Ph.D.

Current
Craig
D
Ellermeier
Ph.D.
Associate Professor
Microbiology
Research area(s): 
Bacterial cell signaling
Address
540M
Eckstein Medical Research Building
540 M
EMRB
Research
Research Focus: 

Work in the Ellermeier Lab focuses on how Gram-positive bacteria sense and respond to extracellular signals. Our work is focused on the opportunistic human pathogen Clostridium difficile and the model organism Bacillus subtilis.  We are interested in understanding how cells respond to changes in their environment by altering gene expression. To alter gene expression bacteria must detect changes in their environment and then transduce that signal from outside the cell to a transcriptional response inside the cell. We are interested in understanding the basic molecular mechanisms involved in how cells sense and respond to extracellular signals. We utilize genetic, molecular, biochemical and structural approaches to dissect these signal transduction systems.

We are particularly interested in understanding the response of C. difficile to factors produced by the innate immune system. Our work has revealed the presence of an Extra Cytoplasmic Function (ECF) σ factor, σV, present in C. difficile and B. subtilis as well as other Gram-positive bacteria that is activated specifically by lysozyme, an essential component of the innate immune system. We have found that σV is required for lysozyme resistance in both B. subtilis and C. difficile. The activity of σV is inhibited by the anti-sigma factor RsiV. Activation of σV occurs via proteolytic destruction of an anti-sigma factor RsiV. This degradation occurs only in the presence of lysozyme and requires multiple proteases to destroy RsiV in a process of regulated intramembrane proteolysis (RIP). We are interested in identifying the proteases required for σV activation and understanding the mechanism by which site-1 cleavage of RsiV, and thus σV activation, is controlled. We are also studying the role of additional ECF sigma factors encoded by C. difficile to determine their role in response to cell envelope stress. In addition, we are interested in understanding the role of these ECF sigma factors play in survival of the bacterium during an infection.

 

Charles Brenner Ph.D.

Current
Charles
Brenner
Ph.D.
Professor and Head
Biochemistry & Internal Medicine
Research area(s): 
Metabolic Control of Gene Expression
Address
4-403
BSB
4-339
BSB
Research
Research Focus: 

Cellular function and differentiation depend on an ability to read environmental cues and to execute a gene expression program that is appropriate to time, place and context.  Nutrient availability is among the most important signals to which cells respond.  Importantly, nutrients are not only transmitted from outside an organism, i.e., by feeding, but are also transmitted from cell to cell and from tissue to tissue.  Metabolic control of gene expression is critical to the maintenance of cellular longevity.  Dysregulation of the nutritional control of gene expression underlies a series of conditions including nondetection of satiety, which can lead to obesity and diabetes, and diseases such as cancer.

Our laboratory is engaged in several projects that dissect specific problems in the metabolic control of gene expression.  In particular, we are interested in how changing environmental conditions lead to reversible transfer of two carbon, i.e. acetyl, and one carbon, i.e. methyl, groups to proteins and DNA, respectively.  These processes are fundamentally important because two carbon transfers link carbohydrate and fat metabolism to nicotinamide adenine dinucleotide (NAD) biosynthesis and because one carbon transfers link the folate cycle and methionine biosynthesis to S-adenosyl methionine metabolism. Trainees in our group are engaged in interdisciplinary projects, performing protein purification, enzymology, structural biology, yeast and somatic cell genetics, genomics, and chemical biology.

Tina Tootle Ph.D.

Current
Tina
Tootle
Ph.D.
Associate Professor
Anatomy and Cell Biology
Research area(s): 
Understanding the mechanisms of prostaglandin signaling
Address
Research
Research Focus: 

Prostaglandins are transiently acting hormones that are synthesized at their sites of action by cyclooxygenase (COX) enzymes, the targets of Aspirin and Advil, to mediate a variety of biological activities, including inflammation, sleep, reproduction, and cancer development. How do prostaglandins regulate these diverse, cellular events? To address this question we have developed Drosophila oogenesis as a new a new and powerful model for studying prostaglandin signaling. Using both pharmacology and genetics, we discovered that prostaglandins mediate Drosophila follicle development, identified the Drosophila COX1 enzyme, Pxt, and revealed that genetic perturbation of prostaglandin signaling can be used to exam the function of prostaglandins. This research on prostaglandin signaling implicates it in modulating actin/membrane dynamics, cell migration, stem cell activity, and the timing of gene expression during Drosophila follicle development. The lab is currently pursuing how prostaglandin signaling regulates actin dynamics and invasive cell migrations during Drosophila follicle development. By using a multifaceted experimental approach that combines Drosophila genetics, cell biology, live imaging, and biochemistry to we can begin to work out the mechanisms by which prostaglandins regulate these processes, and provide general insight into how prostaglandins regulate the cytoskeleton and migration at a cellular level. Such mechanisms of prostaglandin action are likely to be reutilized throughout development, including mediating the changes that occur during cancer progression and metastasis.

Yi Xing Ph.D.

Associate Professor
Internal Medicine

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