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Carol Wilusz


Office: B407 Micro
Office Phone: (970) 491-4919

​Director​​ Molecular Quantification Core​
​Associate Director Graduate Program in Cell & Molecular Biology​
​Associate Director GAUSSI Training Program (Computational Biology and Biosensing)​
​Associate Editor Wiley Interdisciplinary Reviews - RNA
Academic Editor​ PLoS One
Section Editor ​ BBA - Gene Regulatory Mechanisms


MIP611: Advanced Microbiological Research Methods (4CR, Spring)

MIP565: Next Generation Sequencing Platforms & Libraries (1CR, Fall Lab)

CM700: Critical Analysis of the Literature (1CR, Spring & Fall)

CM505: Nucleic Acids for Non-Life Scientists (1Cr, Fall Lab)


BS Biochemistry (1991) Imperial College, London UK

PhD Drosophila Genetics (1995) Imperial College, London UK. 

Research Interests

Our laboratory studies the regulation of mRNA metabolism in eukaryotic cells. Specifically, we are investigating how mRNA turnover influences disease and development. Our interests range from genetic diseases such as myotonic dystrophy, to stem cell biology and infectious disease. Much of the work in my lab is performed in collaboration with Dr Jeffrey Wilusz.  We also collaborate with researchers working on mycobacterial infections including Dr Mercedes Gonzalez-Juarerro (CSU) and Dr Nicholas Walter (National Jewish Health).

MYOTONIC DYSTROPHY:  We are interested in a potential contribution of aberrant mRNA decay to the pathogenesis of Myotonic Dystrophy. Myotonic Dystrophy, DM1, is caused by an expanded CTG repeat in the 3'UTR of the myotonic dystrophy protein kinase (DMPK). RNA containing this repeated sequence acts as a sink for RNA-binding proteins, sequestering them away from their normal functions in splicing, and mRNA decay. Our lab is interested in learning how the mutant DMPK RNA is metabolized in DM1 patient cells, and in uncovering new connections between pathogenesis and the RNA-binding proteins whose function is affected by the toxic DMPK RNA.

COORDINATING GENE EXPRESSION THROUGH RNA MODIFICATION: Post-transcriptional modifications such as the poly(A) tail and N6-methyladenosine can dramatically influence the life span and function of an mRNA molecule.  While the entire population of mRNAs transcribed from a single gene can share the same core sequences, each mRNA within that population may be modified to a different extent.  Changing the level of modification can allow a rapid and coordinated increase or decrease in gene expression in response to cellular stimuli.  We are using standard molecular approaches and next generation sequencing to understand how poly(A) tail length and RNA methylation are regulated in stem and cancer cells. ​


PubMed for Carol Wilusz​

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1682 Campus Delivery
Fort Collins, Colorado 80523-1682

(970) 491-6144

(970) 491-0603