Dr. Laura Newcomb
Assistant Professor
Office: BI 320
Lab: BI 322
Phone: 909 537-5542
e-mail: lnewcomb@csusb.edu
B.S., Biology, Minor in Chemistry, University of Wisconsin - Milwaukee
Ph.D., Biomolecular Chemistry, University of Wisconsin - Madison
NIH Postdoctoral Fellow, Institute for Cellular and Molecular Biology, University of Texas at Austin
Courses:
BIOL 400 Molecular Biology
BIOL 572 Virology
Research Interests:
Viruses are unique in that they are genetic entities which cannot reproduce on their own. In order to reproduce, a virus must infect a host cell and take control of that host cell for its own objectives; mainly to churn out new viral particles. For that reason, there is debate on whether or not viruses can be classified as "living." However, there is no debate that some viruses can cause both health and economic hardships for human populations. On a brighter side, since viruses utilize cellular machinery to replicate, they have long been used as tools for elucidating cellular mechanisms. In fact, in the famous "Hershey-Chase" experiment carried out in 1952, a bacteriophage (virus which infects bacteria) was used to demonstrate that DNA contains genetic information.
Research in my laboratory aims to understand how influenza virus hijacks our cellular machinery in order to reproduce. Influenza virus accounts for over 36,000 deaths each year in the United States alone. Human infection with highly pathogenic H5N1 avian influenza in Asia, Europe, and Africa has prompted alarm that a mutation or recombination event will lead to the emergence of a highly pathogenic easily transmissible strain that will cause a pandemic. Influenza pandemics have occurred at three times in the past century (1918, 1957 and 1968) and our lack of preparation for a possible avian influenza outbreak makes it painfully evident that more knowledge of the basic molecular activities required for influenza replication is needed. Experiments performed in my laboratory will utilize non-virulent lab strains of influenza A virus to address fundamental mechanisms of influenza viral replication.
One area of research will focus on the influenza Nucelocapsid protein which has greater than 90% protein sequence homology among influenza A isolates and plays an essential role in regulating influenza viral RNA replication through its interaction with the influenza viral RNA dependent RNA polymerase. This molecular interaction between the viral Nucleocapsid protein and the viral polymerase is a potential antiviral target, and thus defining these molecular contacts may lay foundation for development of antiviral therapies.
A second area of research aims to identify host RNA processing and nuclear export pathways hijacked by influenza RNAs during viral infection. Influenza transcribes its messenger RNA in the nucleus and requires splicing of two transcripts and export of three distinct classes of viral mRNA; spliced, unspliced intron-containing, and intron-less. At present the cellular export pathway, or pathways, utilized by influenza viral mRNAs remains unknown. This area of research may not only expose antiviral targets, but also has the potential to lead to the discovery of novel cellular RNA processing and nuclear export pathways.
Publications:
Newcomb, L.L., Kuo R.L., Ye Q., Jiang Y., Tao J. and Krug R.M. Interaction of the influenza A virus nucleocapsid protein with the viral RNA polymerase potentiates unprimed viral RNA replication. In review.
Laabs, T. L., Markwardt D. D., Slattery M.G., Newcomb, L.L, Stillman D.J., and Heideman W. ACE2 is required for daughter cell-specific G1 delay in Saccharomyces cerevisiae. Proc Natl Acad Sci U S A. 2003. 100(18): p. 10275-80.
Newcomb L.L., Diderich J.A., Slattery M.G., and Heideman W. Glucose regulation of Saccharomyces cerevisiae cell cycle genes. Eukaryot Cell. 2003. 2(1): p. 143-9.
Newcomb L.L., Hall D.D., and Heideman W. AZF1 is a glucose-dependent positive regulator of CLN3 transcription in Saccharomyces cerevisiae. Mol Cell Biol. 2002. 22(5): p. 1607-14.
Wu M., Newcomb L., and Heideman W. Regulation of gene expression by glucose in Saccharomyces cerevisiae: a role for ADA2 and ADA3/NGG1. J Bacteriol. 1999. 181(16): p. 4755-60.
Brantner C.A., Buchholz L.A., McSwain C.L., Newcomb L.L., Remsen C.C., and Collins, M.L.P. Intracytoplasmic membrane formation in Methylomicrobium album BG8 is stimulated by copper in the growth medium. Can. J. Microbiol. 1997. 43: p. 672-676.
