Microbiology News

Microbiology’s Dokland named ASM Distinguished Lecturer

DoklandTerje Dokland, Ph.D., of the University of Alabama at BirminghamDepartment of Microbiology, has been named an American Society for Microbiology Distinguished Lecturer for 2017-2019. Dokland, a UAB associate professor, studies the structural biology of viral assembly and bacterial pathogenicity, using tools like cryo-electron microscopy and X-ray crystallography.

Beginning July 1, he will join a group of scientifically diverse lecturers who speak at American Society for Microbiology Branch meetings throughout the United States. Frances Lund, Ph.D., UAB chair of Microbiology, called Dokland’s appointment “a national honor.” Read more ...

Genetic clues to kidney disease uncovered

Briles.AAASUsing international genomic studies backed by proof-of-concept cell experiments, researchers have identified two genes that contribute to the chronic kidney disease glomerulonephritis.

This provides new genetic clues to understanding IgA nephropathy, an autoimmune kidney disease that commonly causes kidney failure. The findings are relevant to IgA nephropathy and other diseases with similar underlying molecular defects, such as inflammatory bowel disease, certain types of blood disease and cancer.

“Very little is known about the causes of IgA nephropathy, genetic or otherwise, so our discovery represents an important step toward developing better therapies for this disease,” said lead author Krzysztof Kiryluk, M.D., the Herbert Irving Assistant Professor of Medicine at Columba University Medical Center. Read more ...

Majoring in defense: UAB’s new Undergraduate Immunology Program

Briles.AAASIt doesn’t matter whether you live in Beverly Hills or a Brazilian favela — every human being is only a few inches away from disaster. From birth to death, on our arms, legs and everywhere else, each of us carries microbes that would love to get under our skin and reproduce, with potentially fatal results. A paper cut, an insect bite, an untimely rubbing of the eyes — it takes very little for bacteria, viruses and other invaders to get inside and start wreaking havoc. Read more ...

Three UAB faculty members selected as fellows by world’s largest general scientific society

Briles.AAASFaculty members from the University of Alabama at Birmingham’s College of Arts and Sciences and School of Medicine have been named fellows of the American Association for the Advancement of Science.

The AAAS is the world’s largest multidisciplinary scientific society and a leading publisher of cutting-edge research through its Science family of journals.

Charles Amsler, Ph.D., professor in the College of Arts and Sciences’ Department of Biology, Steven Austad, Ph.D., distinguished professor and chair of the Department of Biology, and David Briles, Ph.D., professor in the School of Medicine’s Department of Microbiology and Department of Pediatrics, are UAB’s three representatives in the 2016 class of AAAS fellows. Read more ...

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Bedwell11

David M. Bedwell, Ph.D.
Professor
Department of Microbiology

Telephone: (205) 934-6593
Office Location: BBRB 432A, zip 2170
Email:  dbedwell@uab.edu

Research Focus:  Translation termination;
nonsense-mediated mRNA decay; genetic diseases



Biography


David Bedwell (b. 1956), Professor of Microbiology, completed his undergraduate studies in Microbiology at Purdue University (B.S. with Honors, 1979). His graduate work was done with Dr. Masayasu Nomura at the University of Wisconsin-Madison, (Ph.D., 1985) and a postdoctoral fellowship was carried out in Dr. Scott Emr's laboratory at Caltech. Dr. Bedwell joined the faculty at UAB in 1988. At the national level, he previously served as chair of the Molecular Genetics C (MGC) Study Section at the National Institutes of Health (NIH), now serves as chair of the Molecular Genetics B (MGB) Study Section. His outside interests include his family and sports.

Lab Research Focus


A major objective of research in Dr. Bedwell’s lab is to understand the mechanistic details of translation termination in eukaryotes. Besides the release factors eRF1 and eRF3, many other cellular components influence the process of translation termination. Surprisingly sophisticated cellular machineries also regulate the abundance of mRNAs based on the location of stop codons. We are using a combination of genetics, biochemistry, and cell biology in a yeast experimental system to better understand the molecular details of how these processes are carried out.

We are also investigating whether pharmacological agents can be used to suppress nonsense mutations that cause genetic diseases.  First, we are exploring whether this novel therapeutic approach can benefit patients with cystic fibrosis (CF).  CF is caused by mutations in the CFTR gene (which corresponds to the mouse Cftr gene).  We have published several papers demonstrating that drugs can suppress nonsense mutations in the CFTR gene in various CF experimental systems, including cultured CF cell lines and a CF mouse expressing a human CFTR-G542X transgene.  Most recently, we have constructed a new Cftr-G542X knock-in mouse model to explore this approach in a more physiologically relevant context.

We are also investigating whether this therapeutic approach can benefit patients with the lysosomal storage disease mucopolysaccharidosis type I-H (MPS I-H, or Hurler syndrome).  MPS I-H is caused by mutations in the human IDUA gene (which corresponds to the mouse Idua gene).  We have constructed a Idua-W392X knock-in mouse and have preliminary evidence that nonsense suppression can partially alleviate the primary biochemical defect that causes this devastating genetic disease.

Finally, the availability of these knock-in mouse models for CF and MPS I-H will allow us to explore whether the suppression of Nonsense-Mediated mRNA Decay (NMD) can further enhance the therapeutic effect provided by nonsense suppression agents.  It is hoped that either nonsense suppression alone or in combination with NMD suppression will ultimately provide a therapeutic benefit for a broad range of human genetic diseases caused by nonsense mutations.