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Annie Zemper

Annie Zemper

Assistant professor, Biology
Member, IMB

Ph.D., Oregon Health and Science University
B.A., Concordia University

Email
Office: 218 Streisinger Hall
Office Phone: 541-346-2403
Lab: 215A-C Streisinger Hall
Lab Phone: 541-346-2065

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Research Interests



Research in the Zemper lab focuses on small intestinal and colonic epithelial stem cell behavior. The intestinal epithelium is a highly dynamic tissue. Normal homeostasis requires intricate control of stem and progenitor cell proliferation, differentiation, migration and ultimately death and detachment. There are several unique populations of progenitor cells within the colonic crypt, and it is posited that each has a unique ability to differentially regulate intestinal homeostasis. These populations are marked by a number of different proteins and have different proliferative properties. The dynamic nature of these intestinal stem cells is likely exploited in normal process of development or repair after injury, but also in malignant transformation.

Our previous research has shown that Leucine rich repeats and immunoglobulin-like domains 1 (Lrig1), a pan-ErbB negative regulator, marks a distinct population of largely quiescent intestinal stem cells and the protein functions as a growth repressor. These discoveries about the Lrig1+ stem cell population tell us something about the role of the cells within the normal small intestinal and colonic crypts in regulating powerful growth factor signaling cascades, as well as inform us about the potential of both Lrig1 and Lrig1-expressing cells in epithelial repair and regeneration after injury. It is unknown how manipulation of one stem cell population affects the colonic tissue repair process in other stem or progenitor populations. Some fundamental questions we address are:

The general approach of our research is to apply sophisticated mouse modeling with ex vivo crypt manipulations (organoid culture) coupled with high, or super-resolution microscopy and large-scale genomic scans to address the fundamental questions proposed above. Our studies take advantage of our unique ability to engineer cellular changes within the niche and directly examine effects on the stem cells and influences downstream on the niche. By employing both in vivo and ex vivo approaches, we hope to decipher the molecular cues important for intestinal stem cell maintenance and how these cues may go awry in disease states, such as inflammatory bowel disease and cancer.

figure 1
The colonic epithelium (stem, transit-amplifying and differentiated cells) is dependent upon proper regulation of signaling cascades, which direct cell division, migration and maintenance. There is cross-talk between the stromal cells (brown) and the epithelium. Together, the stromal cells and the epithelium achieve proper barrier function. Colors in crypt illustration (left) coordinate with the lineage tree (right).
figure 2
Cross-section of a distal portion of a mouse colon from an induced Lrig1-CreERT2/+;R26R-YFP mouse. U-shaped crypts are made of a single layer of epithelial cells, surrounded by supporting cells. In this lineage labeling experiment, some crypts have undergone genetic recombination to reveal daughter cells of Lrig1-expressing progenitors. These crypts express yellow fluorescent protein (green). All cells in the image are labeled with DAPI (purple).

Recent publications

(pulled from pubmed)

Recent publications

(pulled from pubmed)

LRIG1 Regulates Ontogeny of Smooth Muscle-Derived Subsets of Interstitial Cells of Cajal in Mice.
Kondo J, Powell AE, Wang Y, Musser MA, Southard-Smith EM, Franklin JL, Coffey RJ
Gastroenterology 2015 Aug;149(2):407-419.e8
Inducible loss of one Apc allele in Lrig1-expressing progenitor cells results in multiple distal colonic tumors with features of familial adenomatous polyposis.
Powell AE, Vlacich G, Zhao ZY, McKinley ET, Washington MK, Manning HC, Coffey RJ
Am J Physiol Gastrointest Liver Physiol 2014 Jul 1;307(1):G16-23
Using a new Lrig1 reporter mouse to assess differences between two Lrig1 antibodies in the intestine.
Poulin EJ, Powell AE, Wang Y, Li Y, Franklin JL, Coffey RJ
Stem Cell Res 2014 Nov;13(3 Pt A):422-30
Helicobacter pylori promotes the expression of Krüppel-like factor 5, a mediator of carcinogenesis, in vitro and in vivo.
Noto JM, Khizanishvili T, Chaturvedi R, Piazuelo MB, Romero-Gallo J, Delgado AG, Khurana SS, Sierra JC, Krishna US, Suarez G, Powell AE, Goldenring JR, Coffey RJ, Yang VW, Correa P, Mills JC, Wilson KT, Peek RM Jr
PLoS One 2013;8(1):e54344
Pathology of rodent models of intestinal cancer: progress report and recommendations.
Washington MK, Powell AE, Sullivan R, Sundberg JP, Wright N, Coffey RJ, Dove WF
Gastroenterology 2013 Apr;144(4):705-17
The pan-ErbB negative regulator Lrig1 is an intestinal stem cell marker that functions as a tumor suppressor.
Powell AE, Wang Y, Li Y, Poulin EJ, Means AL, Washington MK, Higginbotham JN, Juchheim A, Prasad N, Levy SE, Guo Y, Shyr Y, Aronow BJ, Haigis KM, Franklin JL, Coffey RJ
Cell 2012 Mar 30;149(1):146-58
Fusion between Intestinal epithelial cells and macrophages in a cancer context results in nuclear reprogramming.
Powell AE, Anderson EC, Davies PS, Silk AD, Pelz C, Impey S, Wong MH
Cancer Res 2011 Feb 15;71(4):1497-505
Lessons from development: A role for asymmetric stem cell division in cancer.
Powell AE, Shung CY, Saylor KW, Müllendorff KA, Weiss JB, Wong MH
Stem Cell Res 2010 Jan;4(1):3-9
Characterization of the intestinal cancer stem cell marker CD166 in the human and mouse gastrointestinal tract.
Levin TG, Powell AE, Davies PS, Silk AD, Dismuke AD, Anderson EC, Swain JR, Wong MH
Gastroenterology 2010 Dec;139(6):2072-2082.e5
Inflammation and proliferation act together to mediate intestinal cell fusion.
Davies PS, Powell AE, Swain JR, Wong MH
PLoS One 2009 Aug 6;4(8):e6530
Wnt-reporter expression pattern in the mouse intestine during homeostasis.
Davies PS, Dismuke AD, Powell AE, Carroll KH, Wong MH
BMC Gastroenterol 2008 Dec 2;8:57