John J. Karijolich, Ph.D.a

Assistant Professor

Dept. of Pathology, Microbiology and Immunology

Contact Information

Office Location:

A-4301 MCN

Phone: 615-875-7686

E-mail: john.karijolich@vanderbilt.edu

Lab URL:

Karijolich Lab

Campus Mail address:

Pathology, Microbiology and Immunology-5th Fl

A-5301 MCN (2363)

US Mailing address:

Vanderbilt University School of Medicine

Dept Pathology, Microbiology and Immunology-5th Fl

A-5301 MCN

Nashville, TN 37232-2363

Research Specialty


Host-pathogen interaction, noncoding RNA, innate immunity, endogenous retroviruses, retrotransposons, herpesviruses, gene expression, virology, cancer.

Research Description


The association between infection with viruses and neoplasia is well established for a variety of cancers. In fact, approximately 12% of human cancers worldwide are caused by oncogenic viral infections, with more than 80% of cases occurring in the developing world. Despite their prevalence and public health importance, our understanding and ability to manage viral-induced cancers is still limited. This is in part due to the complexity of host-virus interactions leading to cellular transformation. Research in our laboratory is focused on defining the host-virus interaction in the context of gammaherpesviral infection. γ-herpesviruses, which include the human oncogenic viruses Kaposi Sarcoma-associated herpesvirus (KSHV) and Epstein Barr virus (EBV), are a family of large double-stranded DNA lymphotrophic viruses that are the causative agents of a variety of disorders, including lymphoproliferative diseases, lymphomas, as well as other nonlymphoid cancers in mammals. Studies of the host response to viral infection have historically focused on protein-coding genes, thus our understanding of how the non-protein-coding transcriptome, including both viral- and host-derived noncoding RNAs, impacts host-virus interactions is limited. Along this line, our primary research goals are directed towards understanding how noncoding RNAs and their RNA-binding proteins are integrated in to the regulation of gene expression and modulation of the host immune response during γ-herpesviral infection. To accomplish this we undertake a multidisciplinary approach combining virology, immunology, RNA biochemistry, proteomics, and genomics/transcriptomics. Major thematic questions of the lab include:

1) What are the endogenous and exogenous noncoding RNA species that contribute to innate immune modulation and how are these functions mediated?

2) How does the cell intrinsic innate immune system shape the γ-herpesviral lifecycle and what are the host and viral entities at play?

3) What is the contribution of endogenous retroviruses and transposons to the host-virus interaction?

Publications

  1. Huang C, Karijolich J, Yu YT. Detection and quantification of RNA 2'-O-methylation and pseudouridylation. Methods 2016 Feb 4.

  2. Karijolich J, Abernathy E, Glaunsinger BA. Infection-induced retrotransposon-derived noncoding RNAs enhance herpesviral gene expression via the NF-κB pathway. PLoS Pathogens. 2015 Nov. 19; 11(11)

  3. Karijolich J*, Yi C, Yu YT*. Transcriptome-wide dynamics of RNA pseudouridylation. Nat. Rev. Mol. Cell Biol. 2015 Aug 19. doi: 10.1038/nrm4040., *Co-corresponding authors

  4. Karijolich J*, Yu YT*. The new era of RNA modifications. RNA. 2015 Apr;21(4):659-60. *Co-corresponding authors

  5. Jun Lim S, Scott A, Xiong XP, Vahidpour S, Karijolich J, Guo D, Pei S, Yu YT, Zhou R, Li W. Requirement for CRIF1 in RNA interference and Dicer-2 stability. RNA Biol. 2014. Nov; 9:1171-9

  6. Karijolich J*, Yu YT*. Therapeutic suppression of premature termination codons: mechanisms and clinical considerations. Int J Mol Med. 2014. Aug; 34(2):355-62. *Co-corresponding authors

  7. Karijolich J, Zhao Y, Peterson B, Zhou Q, Glaunsinger B. Kaposi's sarcoma-associated herpesvirus ORF45 mediates transcriptional activation of the HIV-1 long terminal repeat via RSK2. J Virol. 2014. Jun; 88(12):7024-35.

  8. Karijolich JJ, Hampsey M. The Mediator complex. Curr Biol. 2012 Dec 18;22(24): R1030-1

  9. Karijolich J*, Yu YT. Converting nonsense codons into sense codons by targeted pseudouridylation. Nature. 2011 474:395-8. *Highlighted in News & Views in same issue of Nature 474:289-290.

  10. Huang C, Karijolich J, Yu YT. Post-transcriptional modification of RNAs by artificial Box H/ACA and Box C/D RNPs. Methods Mol Biol. 2011; 718:227-44

  11. Karijolich J, Kantartzis A, Yu YT. RNA modifications: a mechanism that modulates gene expression. Methods Mol Biol. 2010; 629:1-19

  12. Karijolich J, Kantartzis A, Yu YT. Quantitative analysis of RNA modifications. Methods Mol Biol. 2010; 629:21-32

  13. Karijolich J, Yu YT. Spliceosomal RNA modifications and their function. RNA Biol. 2010 7:192-204

  14. Karijolich J, Huang C, Yu YT. Enzymes responsible for spliceosomal snRNA pseudouridylation. In: DNA and RNA Modification Enzymes: Comparative Structure, Mechanism, Functions, Cellular Interactions and Evolution. (ed. H. Grosjean) p.461-474. 2009.

  15. Karijolich J, Yu YT. Pre-mRNA splicing. In Encyclopedia of Chemical Biology (ed. TP Begley). DOI:10.1002/9780470048672.wecb520. Article Online Posting Date: March 14th, 2008

  16. Stephenson D, Karijolich J, Yu YT. Functional roles of spliceosomal snRNA modifications in pre-mRNA splicing. In: RNA and DNA editing: Molecular mechanisms and their integration into biological systems. (ed. H. Smith) Hoboken, New Jersey: Wiley-Interscience. 175-189. 2008

  17. Karijolich J, Yu YT. Insight into the protein components of the Box H/ACA RNP. Current Proteomics 2008; 5: 129-137

  18. Karijolich J, Stephenson D, Yu YT. Biochemical Purification of box H/ACA RNPs involved in pseudouridylation. Methods Enzymol 2007; 425:241-62

  19. Moelling C, Oberschlacke R, Ward P, Karijolich J, Borisova K, Bjelos N, and Bergeron L. Metal-dependent repression of siderophore and biofilm formation in Actinomyces naeslundii. FEMS Microbiol Lett. 2007; 2:214-20