Faculty

John E. Linz , Professor & Associate Chairperson

Postdoctoral, University of California at Irvine, 1986
Postdoctoral, University of Illinois, 1984
Ph.D., Louisiana State University, 1983
M.S., University of Illinois, 1979

234B G.M. Trout FSHN Building
Michigan State University
East Lansing, MI 48824-1224
Phone: (517) 355-8474, Ext. 126
Lab: (517) 355-8474, Ext. 162
Fax: (517) 353-8963
E-mail: jlinz@msu.edu

Research Interests: 

Campylobacter jejuni is the most prevalent causative agent of bacterial food borne disease in the Unite States. Up to 4 million disease cases, over 100 deaths, and billions of dollars in direct and indirect costs are associated with human infection annually prompting widespread concern. In response to this concern, C. jejuni was listed as a Category B Priority Pathogen within NIAID’s Biodefense Research Initiative. Although virulence factors are reported to play a role in the disease process (eg. cytolethal distending toxin and flagella), these alone are not likely sufficient to explain the impressive disease statistics. We propose that two genetic processes explain, at least in part, C. jejuni’s unique prowess as a pathogen: 1) C. jejuni generates striking genetic diversity in several contingency genes by slip strand mutagenesis (mutations in up to 50 percent of the cells in the population); and 2) C. jejuni transfers genetic material to other cells in a population with a high degree of specificity and at high frequency via natural transformation (NT). The hypothesis is that these two engines of genetic diversity, rapidly generate sub-populations of C. jejuni with novel combinations of genetic traits (antibiotic resistance markers, virulence genes, immunogenic surface molecules) allowing bacterial cells to adapt to a wide variety of host environments; this adaptation results in cells with enhanced ability to evade or alter the host immune response, to invade tissue in the GI tract, and to generate acute and chronic disease symptoms. Our long-term goal is to understand the association between genetic diversity and virulence in C. jejuni. The short-term goal is to develop a better understanding of the genetic mechanisms that drive genetic diversity in C. jejuni. To obtain this goal we are currently pursuing the following specific aims: 1) Explore the role of uptake sequences and competence genes in NT. 2) Measure rates of NT of antibiotic resistance genes, virulence genes and contingency genes in animal models (mice [colonization and disease] and chickens [colonization only]) of the human GI tract. 3)  Measure the frequency of mutation in contingency genes in the animal models.  Determine the frequency of specific genotypes and range of different genotypes among animal isolates. The basic knowledge derived from these studies should directly increase our understanding of the disease process and be applicable to the development of measures to prevent and alleviate disease and its debilitating sequellae in humans. 

Aflatoxins are biologically active secondary metabolites that frequently contaminate food and feed crops such as peanuts, treenuts, corn, cottonseed; the annual cost of detecting and diverting contaminated crops is estimated at nearly $500,000,000 annually in the United States. Our goal is to identify novel and effective procedures to reduce or eliminate aflatoxin contamination. We are currently conducting research in several related areas: 1) Understand the structure and function of aflatoxin gene promoters including identification and characterization of novel transcription factors. 2) Understand the gene cluster effects on aflatoxin gene expression at the level of chromatin remodeling. 3) Understand the role of cAMP and ethylene signaling pathways in regulation of aflatoxin synthesis. 4) Understand the physical interaction of the aflatoxin enzymes and their localization with fungal colonies and cells.

Instructional Activities:

FSC 440 – Food Microbiology
FSC 840 – Advanced Food Microbiology
FSC 441 – Food Microbiology Laboratory

Recent Publications:

Lee JW, Miller MJ, Roze LV, and Linz JE.  2007.  "A wortmannin-sensitive signal transduction pathway inhibits aflatoxin synthesis."  Mycologi.

Severin J, Bix L, Linz JE, Gilliland D, and Lockhart H.  2007.  "A new methodology for whole package microbial challenge testing for medical device trays."  Journal of  Testing and Evaluation.

Gunterus A, Roze LV, Beaudry R, and Linz JE. 2007. "Ethylene inhibits aflatoxin biosynthesis in Aspergillus parasiticus grown on peanuts."  Food Microbiology.

Mansfield LS, Bell JA, Wilson DL, Murphy AJ, Elsheikha HM, Rathinam VA, Fierro BR, Cortez JS, Linz JE, and Young VB.  2006. "C57BL/6 mice and their syngeneic IL-10 knockout can serve as models of Campylobacter jejuni colonization and enteritis." Infection and Immunity 47:1099-1115.

Siripatrawan U, Linz JE, and Harte BR.  2006. "Detection of E. coli in packaged alfalfa sprouts using electronic nose and an artificial neural network."   J. Food Prot. 69:1844-1850.

Halbert LW, Kaneene JB, Linz JE, Mansfield LS, Wilson, D, Ruegg PL, Warnick LD, Wells SJ, Fossler CP, Campbell AM, Geiger-Zwald AM.  2006. "Genetic mechanisms contributing to reduced tetracycline susceptibility of Campylobacter isolated from organic and conventional dairy farms in the Midwest and Northeast US."  J. Food Prot. 69:482-488

Miller MJ, and Linz JE.  2006. "Genetic mechanisms involved in regulation of mycotoxin biosynthesis." Review.  Food Biotechnology.

Siripatrawan U, Linz JE, and Harte B.  2006.  "Electronic sensor array coupled with artificial neural network for detection of Salmonella Typhimurium."  Sensors and Actuators B 119:64-69.

Moorman M, Nettleton W, Ryser E, Linz JE and Pestka J. "Sanitizer sensitivity of Listeria innocua exposed to acid, cold, heat, and starvation conditions." J. Food Protect. 68:1659-1663, 2005.

Miller MJ and Linz JE. "Genetic mechanisms involved in regulation of mycotoxin biosynthesis." Peer Reviewed, Invited Book Chapter. Food Biotechnology. 2005.

Miller MJ, Rarick M, Roze L, Trail F and Linz JE. "Cis-acting sites, NorL, TATA box, and AflR1 play important roles in nor-1 transcriptional activation in Aspergillus." Appl. Environ. Microbiol. 71:1539-1545, 2005.

*Adobe Acrobat Reader is required to read PDF documents.