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MicroRNA-7 Specifically Marks the Gut Endocrine Lineage and Controls Progenitor Cell Proliferation Through Egfr

34 Pages Posted: 26 Sep 2018 Sneak Peek Status: Review Complete

See all articles by Ajeet P. Singh

Ajeet P. Singh

Cornell University - Department of Biomedical Sciences

Yu-Han Hung

Cornell University - Department of Biomedical Sciences

Alessandro Bonfini

Cornell University - Cornell Institute of Host-Microbe Interactions and Disease

Matthew Kanke

Cornell University - Department of Biomedical Sciences

Michael T. Shanahan

Cornell University - Department of Biomedical Sciences

Michael K. Dame

University of Michigan at Ann Arbor, Medical School, Department of Cell and Developmental Biology

Mandy Biraud

North Carolina State University - Department of Molecular Biomedical Sciences

Bailey C. E. Peck

University of Michigan at Ann Arbor - Department of Surgery

John M. Freund

North Carolina State University - Department of Clinical Sciences

Rebecca L. Cubitt

Cornell University - Department of Biomedical Sciences

Ennessa G. Curry

University of North Carolina (UNC) at Chapel Hill - Department of Cell Biology and Physiology

Liara M. Gonzalez

North Carolina State University - Department of Clinical Sciences

Christopher M. Dekaney

North Carolina State University - Department of Molecular Biomedical Sciences

Gavin A. Bewick

King’s College London - Diabetes Research Group

Natasza A. Kurpios

Cornell University - Department of Molecular Medicine

Shengli Ding

University of North Carolina (UNC) at Chapel Hill - Department of Cell Biology and Physiology

Jason R. Spence

University of Michigan at Ann Arbor, Medical School, Department of Cell and Developmental Biology

Nicolas Buchon

Cornell University - Cornell Institute of Host-Microbe Interactions and Disease

Praveen Sethupathy

Cornell University - Department of Biomedical Sciences

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Abstract

Enteroendocrine cells (EECs) are critical for orchestrating proper responses to nutritional and microbial input. Importantly, EEC progenitors exhibit stem cell potential and contribute to intestinal epithelial proliferation; however, the molecular mechanisms are not well understood. In this study, we first report that miR-7 is a highly specific marker of the EEC lineage and is the most enriched miRNA in Prox1+ EEC progenitors. Next, we show that miR-7 is functionally suppressed in EEC progenitors by pro-proliferative perturbations in mouse and fruit fly. We then demonstrate that miR-7 exerts highly conserved control of intestinal epithelial proliferation and further show that miR-7 regulates the balance between proliferation and differentiation in murine EEC progenitors. Importantly, we also provide the mechanistic insight that miR-7 function is mediated by suppression of Egfr signaling. Overall, this study uncovers a novel role for miRNAs, specifically miR-7, in marking the EEC lineage and controlling the behavior of EEC progenitors.

Suggested Citation

Singh, Ajeet P. and Hung, Yu-Han and Bonfini, Alessandro and Kanke, Matthew and Shanahan, Michael T. and Dame, Michael K. and Biraud, Mandy and Peck, Bailey C. E. and Freund, John M. and Cubitt, Rebecca L. and Curry, Ennessa G. and Gonzalez, Liara M. and Dekaney, Christopher M. and Bewick, Gavin A. and Kurpios, Natasza A. and Ding, Shengli and Spence, Jason R. and Buchon, Nicolas and Sethupathy, Praveen, MicroRNA-7 Specifically Marks the Gut Endocrine Lineage and Controls Progenitor Cell Proliferation Through Egfr (September 26, 2018). Available at SSRN: https://ssrn.com/abstract=3255559 or http://dx.doi.org/10.2139/ssrn.3255559
This is a paper under consideration at Cell Press and has not been peer-reviewed.

Ajeet P. Singh

Cornell University - Department of Biomedical Sciences

NY
United States

Yu-Han Hung

Cornell University - Department of Biomedical Sciences

NY
United States

Alessandro Bonfini

Cornell University - Cornell Institute of Host-Microbe Interactions and Disease

Ithaca, NY 14853
United States

Matthew Kanke

Cornell University - Department of Biomedical Sciences

NY
United States

Michael T. Shanahan

Cornell University - Department of Biomedical Sciences

NY
United States

Michael K. Dame

University of Michigan at Ann Arbor, Medical School, Department of Cell and Developmental Biology

Ann Arbor, MI
United States

Mandy Biraud

North Carolina State University - Department of Molecular Biomedical Sciences

Hillsborough Street
Raleigh, NC 27695
United States

Bailey C. E. Peck

University of Michigan at Ann Arbor - Department of Surgery

500 S. State Street
Ann Arbor, MI 48109
United States

John M. Freund

North Carolina State University - Department of Clinical Sciences

Hillsborough Street
Raleigh, NC 27695
United States

Rebecca L. Cubitt

Cornell University - Department of Biomedical Sciences

NY
United States

Ennessa G. Curry

University of North Carolina (UNC) at Chapel Hill - Department of Cell Biology and Physiology

102 Ridge Road
Chapel Hill, NC 27514
United States

Liara M. Gonzalez

North Carolina State University - Department of Clinical Sciences

Hillsborough Street
Raleigh, NC 27695
United States

Christopher M. Dekaney

North Carolina State University - Department of Molecular Biomedical Sciences

Hillsborough Street
Raleigh, NC 27695
United States

Gavin A. Bewick

King’s College London - Diabetes Research Group

Strand
London, England WC2R 2LS
United Kingdom

Natasza A. Kurpios

Cornell University - Department of Molecular Medicine

Ithaca, NY 14853
United States

Shengli Ding

University of North Carolina (UNC) at Chapel Hill - Department of Cell Biology and Physiology

102 Ridge Road
Chapel Hill, NC 27514
United States

Jason R. Spence

University of Michigan at Ann Arbor, Medical School, Department of Cell and Developmental Biology

Ann Arbor, MI
United States

Nicolas Buchon

Cornell University - Cornell Institute of Host-Microbe Interactions and Disease

Ithaca, NY 14853
United States

Praveen Sethupathy (Contact Author)

Cornell University - Department of Biomedical Sciences ( email )

NY
United States

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