header-logo
AdobeStock_214253348
Michaela Patterson, PhD

Michaela Patterson, PhD

Associate Professor

Locations

  • Cell Biology, Neurobiology & Anatomy
    MEB M4575
    Cardiovascular Center

Contact Information

Education

Postdoctoral Fellowship, University of Southern California, Los Angeles, CA
PhD, University of California, Los Angeles, CA
BS, Bates College, Lewiston, ME

Research Interests

Michaela Patterson, PhD research interests

Our lab’s scientific interests lie at the intersection of cellular ploidy, genetic diversity, basal heart physiology, and tissue repair. We employ a mix of forward genetics approaches and resources to identify novel players in the traits we are exploring, along with classic reverse genetics and engineered animal models to assess causative relationships between identified genes and correlated phenotypes. Some specific areas of interest include:

1) Validation of the genetic underpinnings of cardiomyocyte ploidy and heart regeneration.

Patterson et al., Nature Genetics 2017 examined the relationship between cardiomyocyte ploidy and myocardial regeneration. Using a collection of 120 inbred mouse strains known as the Hybrid Mouse Diversity Panel, we uncovered multiple genetic loci associated with cardiomyocyte ploidy. We went on to validate the causative gene from the first locus, which proved to be Tnni3k.

The Patterson Lab has multiple projects underway (along with others still looking for a project lead) surrounding the other loci to arise from this screen. Using a variety of reverse genetic tools, including genetically engineered mice, viral induction, and more, some of the questions we commonly ask are:

  • Is a candidate gene in the locus responsible for cardiomyocyte ploidy phenotypes AND what role do they play post-MI?
  • Do the candidate genes have “functional” variants and what effect do they have on the gene’s molecular function and on ploidy?
  • How do multiple genes, which individually influence ploidy, act together?
  • Not all candidate genes function in cardiomyocytes, but instead act indirectly through another cell. What other cell types influence cardiomyocyte ploidy and MI outcomes?

2) New genetic screens to identify more players in cardiomyocyte polyploidization and outcomes after heart attack.

Our past work utilized the Hybrid Mouse Diversity Panel, a collection of inbred mouse strains designed to support genome-wide association studies. Our colleagues here at the Medical College of Wisconsin have recently rederived the rat equivalent resource - the Hybrid Rat Diversity Panel. The rat panel has many benefits that make it a superior genetic resource to the mouse panel, most notably that it is four times more genetically diverse. We have multiple projects underway, many of them collaborative, to examine a multitude of phenotypes across the Rat Panel. Phenotypes range from assessment of relevant cell populations to basal heart physiology to outcomes after heart attack and more. This arm of the Patterson lab has endless possibilities for expansion.

3) Polyploidy in other cell types.

Cardiomyocytes are not the only somatic cell in the body that displays substantial polyploidy. By examining the frequency of polyploid cells in other tissues we hope to better understand the overarching function of polyploidy in cell biology and determine if cell types utilize overlapping or distinct molecular mechanisms to drive polyploidization.

4) Bring your own ideas!

We are actively recruiting trainees at the graduate student and postdoctoral levels. We welcome new ideas to transform the way we think about tissue regeneration an repair. If you are interested in joining or rotating in the Patterson Lab, please contact Michaela Patterson, PhD, at mpatterson@mcw.edu.

Publications