Microbiology News

Leon and Lund Discuss Current Research Online

RS14598 Beatriz Leon Ruiz 5 scrFran Lund 14 1
Microbiology’s Beatriz León, Ph.D., and Frances Lund, Ph.D., discuss how exposure to dust mites links to allergies and asthma in MD Magazine online

Researchers identify previously unknown step in the pathway that leads to asthma

Andre Ballesteros Tato Beatriz Leon RuizA team of UAB researchers including microbiology department assistant professor Beatriz León, Ph.D., and her husband, Andre Ballesteros-Tato, Ph.D., (Clinical Immunology and Rheumatology) have identified a previously unknown step in the pathway that leads to asthma. The results of their study are published online, ahead of print, in “T follicular helper cell plasticity shapes pathogenic T helper 2 cell-mediated immunity to inhaled house dust mite.” Read more ...

Kearney Receives AAI-BioLegend Herzenberg Award

john kearney 2013The American Association of Immunologists (AAI) has named microbiology professor John Kearney, Ph.D., the 2016 AAI-BioLegend Herzenberg Award for his outstanding research contributions to the field of immunology in the area of B cell biology.

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24th Annual Microbiology Research Retreat

Written by Peter Burrows, Ph.D.
2015 Retreat Photo by Baiyi Cai 1 ps1aPhoto by Baiyi Cai
November 13-15, 2015, UAB Microbiology Department faculty, postdoctoral fellows, graduate students and special guests gathered in Chattanooga at the Chattanoogan Hotel for our annual research retreat. This year’s retreat—number 24—was once more a wonderful opportunity for members of the department to focus on science and to establish new collaborations away from the distractions of everyday life.
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Calendar

Save the Date


Bertram M. Marx Lecture

Speaker: Roy Curtiss, III, Ph.D.
March 15, 2016 | Noon
Volker Hall LECTURE ROOM B




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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.