Name: Dr. Drew Reams
Title: Assistant Professor in Biological Sciences
Office Location: SQU120C
Office Phone: (916) 278-7678
Mailing Address: Sacramento State, Dept of Biological Sciences, 202 Sequoia Hall, 6000 J street, Sacramento, CA 95819-6077
Office Hours: T/R 10-11:30am in SQU 120-C for Spring '17
Website : www.drewreams.com
Courses That I Teach
BIO 150: Forensic Biology (lecture and lab)
BIO 151: Advanced Laboratory Techniques in Forensic Biology
BIO 180: Advanced Molecular Biology (lecture and lab)
BIO 184: General Genetics (lecture and lab)
BIO 199: Independent Research
BIO 223: Human Molecular Genetics
Research Lab Website
Current Lab Members
Semarhy Quiñones, PhD (Co-Investigator)
Elizabeth Reis (Masters Student)
Reams, A.B. & Roth, J.R., 2015. Mechanisms of gene duplication and amplification In "DNA Recombination". Editors: Stephen Kowalczykowski, Neil Hunter, and Wolf Heyer, Cold Spring Harbor Laboratory Press, Cold Spring Harbor, NY.
Reams, A. B. E. Kofoid, N. Duleba, and J. R. Roth, 2014. “Recombination and annealing pathways compete for substrates in making rrn duplications in Salmonella enterica” Genetics, 196:119-135
Quiñones-Soto S., A. B. Reams, and J.R. Roth, 2012. “Pathways of genetic adaptation: Multi-step origin of mutants under selection without induced mutagenesis in Salmonella enterica” Genetics, 192:987-999.
Reams, A. B. E. Kofoid, E. Kugelberg, and J. R. Roth, 2012. “Formation of duplications by multiple pathways with and without recombination (RecA)” Genetics, 192:397-415.
Reams, A. B., E. Kofoid, M. Savageau, and J. R. Roth, 2010. “Duplication frequency in a population rapidly approaches steady state with or without recombination” Genetics, 184:1077-1094.
Roth, J. R., E. Kugelberg, A. B. Reams, and D.I. Andersson, 2006. “Origins of mutations under selection - the adaptive mutation controversy” Annual Reviews of Microbiology, 13(60), 477-501.
Kugelberg E., E. Kofoid, A. B. Reams, D. I. Andersson, and J. R. Roth, 2006. “Multiple pathways of selected gene amplification during adaptive mutation” PNAS, 2006 Nov 14;103(46):17319-24.
Reams, A. B. and E. L. Neidle, 2004. “Selection for gene clustering by tandem duplication” Annual Reviews of Microbiology, 58, 119-142.
Reams, A. B. and E. L. Neidle, 2004. “Gene amplification involves site-specific short homology-independent illegitimate recombination in Acinetobacter sp. strain ADP1” Journal of Molecular Biology, 338(4), 643-56.
Reams, A. B. and E. L. Neidle, 2003. “Genome plasticity in Acinetobacter: new degradative capabilities acquired by the spontaneous amplification of large chromosomal segments” Molecular Microbiology, 47(5), 1291-1304.
Brzostowicz, P. C., A. B. Reams, T. J. Clark, and E. L. Neidle, 2003. “Transcriptional cross-regulation of the catechol and protocatechuate branches of the b-ketoadipate pathway contributes to carbon-source dependent expression of the Acinetobacter sp. strain ADP1 pobA gene” Applied and Environmental Microbiology, 69(3), 1598-1606.
Links to Publications
Our lab focuses on understanding rapid genetic evolution and copy number variation. Genetic evolution occurs fast when selection and mutation are combined. Many important biological phenomena depend on rapid genetic evolution, such as a pathogen’s acquisition of antibiotic resistance and avoidance of host defenses. In general, this rapid evolution is central to biology and many aspects of medical science, including all infectious diseases and cancer.
A major contributor to rapid genetic evolution is an elusive phenomenon called Copy Number Variation (CNV). CNVs are alterations of a genome that result in an abnormal number of copies of a section of DNA. Unlike point mutations, CNVs are extremely common genetic polymorphisms in all life forms, arising at rates several orders of magnitude higher than point mutations. For example, every human genome contains hundreds of CNVs, many being unique to each individual. Adjusting the copy number of any particular gene changes its expression and results in altered phenotypes, ranging from very subtle to extreme changes. Since CNVs form at very high rates and have phenotypes, they may be expected to play an important role in medicine and evolution. Indeed, in recent years, CNVs have been identified as causing an increasingly large number of human disorders including Alzheimer, Parkinson, autism, schizophrenia, and many other diseases. CNVs can also contribute to resistance and susceptibility to infections, modulate drug responses, and play a central role in oncogenesis and cancer progression. Furthermore, CNVs play a major role in driving the evolution of new genes. Still, the underlying mechanisms of CNVs remain unclear for all organisms.
In order to study rapid evolution and copy number variation, our lab utilizes some of the most genetically tractable organisms: bacteria such as E. coli, Salmonella, and Acinetobacter. The projects are accessible to students at all levels and involve undergraduate and Masters students. Students are trained in important multidisciplinary areas that bridge classical and modern genetics with microbiology, molecular biology, population genetics, experimental evolution, statistics, and computation.