Colin Parrish, PhD
John M. Olin Professor of Virology

Phone

607-256-5649
Fax: 607-256-5608

Address

James A. Baker Institute
Hungerford Hill Road
College of Veterinary Medicine
Cornell University
Ithaca, NY 14853

Email

Web Sites

Background

The basic and applied work of this laboratory are concerned with the study of viral diseases of dogs and cats, and our main efforts have been concentrated on a detailed analysis of parvoviruses of cats, raccoons, mink, and other carnivores, as well a studies to characterize the minute virus of canines.

Research Description

Canine parvovirus (CPV) and the closely related feline panleukopenia virus (FPV) cause a variety of diseases in dogs and cats, with the main signs being diarrhea when the infection occurs in animals older than 2-3 months, while after fetal or neonatal infection myocarditis may occur in puppies or cerebella disease in kittens. In our studies we seek to understand at a very detailed level how these viruses function - which parts of the virus are responsible for the control of viral host range, how they infect cells, and how the immune responses of the host controls the infection. A major aim is to develop better and more effective methods for vaccinating dogs or cats against these viruses.

Selected Publications

Sugawara, N., Goldfarb, T., Studamire, B., Alani, E., and Haber, J. E. (2004)  Heteroduplex  rejection during single-strand annealing requires Sgs1 helicase and mismatch repair  proteins Msh2 and msh6 but not Pms1.  Proc. Natl. Acad. Sci. USA  101, 9315-9320.

Argueso, J. L., Wanat, J., Gemici, Z., and Alani, E.  (2004).  Competing crossover pathways act during meiosis in Saccharomyces cerevisiae.  Genetics, 168, 1805-1816.

Surtees, J., Argueso, J. L., and Alani, E.  (2004).  Mismatch repair proteins: key regulators of genetic recombination. Cytogenetic and Genome Research, 107, 146-159.

Goldfarb, T., and Alani, E. (2005). Distinct roles for the Saccharomyces cerevisiae mismatch repair proteins in heteroduplex rejection, mismatch repair, and non-homologous tail removal.  Genetics 169, 563-574.

Jiang, J., Bai, L., Surtees, J. A., Gemici, Z., Wang, M. D., and Alani, E. (2005).  Detection of high affinity mismatch binding and sliding clamp modes for the MSH2-MSH6 mismatch recognition complex by single-molecule unzipping force analysis. Mol. Cell 20, 771-781.

Lee, S. D., and Alani, E. (2006).  Analysis of interactions between mismatch repair initiation factors and the replication processivity factor PCNA. J. Mol. Biol. 355, 175-184.

Heck, J. A., Argueso, J. L., Gemici, Z., Reeves, G. R., Bernard, A., Aquadro, C. F., and Alani, E. (2006).  Negative epistasis between natural variants of the Saccharomyces cerevisiae MLH1 and PMS1 genes results in a defect in mismatch repair.  Proc. Natl. Acad. Sci. USA 103, 3256-3261.

Surtees J. A., and Alani, E. (2006).  Mismatch Repair Factor MSH2-MSH3 binds and alters the conformation of branched DNA structures predicted to form during genetic recombination.  J. Mol. Biol.  360, 523-536.

Heck, J. A., Gresham, D., Botstein, D., and Alani, E.  (2006).  Accumulation of recessive lethal mutations in S. cerevisiae mlh1 mismatch repair mutants is not associated with gross chromosomal rearrangements.  Genetics 174, 519-523.

Lee, S. D., Surtees, J. A., and Alani, E. (2007). Saccharomyces cerevisiae MSH2-MSH3 and MSH2-MSH6 complexes display distinct requirements for DNA binding Domain I in mismatch recognition.  J. Mol. Biol. 366, 53-66.

Wanat, J. J., Singh, N., and Alani, E. (2007).  The effect of genetic background on the function of Saccharomyces cerevisiae mlh1 alleles that correspond to HNPCC missense mutations.  Hum. Mol. Genet. 16, 445-452.

Gorman, J., Chowdhury, A., Surtees, J. A., Shimada, J., Reichman, D. R., Alani, E., and Greene, E.  Dynamic basis for one-dimensional DNA scanning by the mismatch repair complex Msh2-Msh6. submitted.

Click here for Dr. Alani's PubMed listing.