Presentation Title

Implications of depleting tumor suppressor p73 in adipogenesis

Presenter's Name(s)

Alison ChiversFollow

Time

3:00 PM

Location

Silver Maple Ballroom - Health Sciences

Abstract

Tumor suppressors function to control cell division, allot time for DNA damage repair, and induce programmed cell death, or apoptosis, upon failure of a cell to properly replicate its DNA before cell division. In cancer, tumor suppressor genes are frequently mutated, allowing for uncontrolled cell proliferation, the fundamental characteristic that all types of cancer share. My research involves the investigation of p73, a member of the p53 tumor suppressor protein family, in stem cell biology and examination of pathologies associated with the loss of the p73 gene. Specifically, my project seeks to define the role of p73 in the early phases of adipogenesis, the process of stem cell to adipocyte (fat storing cell) differentiation, by determining how p73 deficiency impairs the normal differentiation pathway of adipocytes. Despite extensive research on the central role of p53 in cellular control and the downstream effects of p53 inactivation, those of its homolog, p73, have yet to be elucidated. Therefore, I explore the transcriptional regulatory activity of p73 with two central hypotheses: 1) that p73 activates signaling pathways that drive stem cell differentiation upon genomic stability; and 2) that p73 deficient stem cells lack the ability to differentiate into mature adipocytes, proposing p73 as a crucial transcription factor in stem cell differentiation, specifically in the process of adipogenesis. Qualitative and quantitative analysis of differences in expression of mesenchymal stem cell (MSC) markers throughout the stages of adipogenesis between wild type (WT) induced pluripotent stem cells (iPSCs) and p73 knock-out (p73KO) iPSCs will provide insight into these hypotheses. Completion of these studies will enhance our understanding of the role of p73 in cellular maturation and will highlight the importance of tumor suppressor activity in preserving the integrity of the human genome.

Primary Faculty Mentor Name

Seth Frietze, PhD

Secondary Mentor Name

Carmen Marín Viera, PhD., Margarita Marqués Martínez, PhD., Marta Martín López, PhD.

Graduate Student Mentors

Diana Gerrard, Princess Rodriguez, Laura Maeso Alonso, Javier Villoch, Angela Diez

Status

Undergraduate

Student College

College of Nursing and Health Sciences

Program/Major

Medical Laboratory Science

Primary Research Category

Health Sciences

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Implications of depleting tumor suppressor p73 in adipogenesis

Tumor suppressors function to control cell division, allot time for DNA damage repair, and induce programmed cell death, or apoptosis, upon failure of a cell to properly replicate its DNA before cell division. In cancer, tumor suppressor genes are frequently mutated, allowing for uncontrolled cell proliferation, the fundamental characteristic that all types of cancer share. My research involves the investigation of p73, a member of the p53 tumor suppressor protein family, in stem cell biology and examination of pathologies associated with the loss of the p73 gene. Specifically, my project seeks to define the role of p73 in the early phases of adipogenesis, the process of stem cell to adipocyte (fat storing cell) differentiation, by determining how p73 deficiency impairs the normal differentiation pathway of adipocytes. Despite extensive research on the central role of p53 in cellular control and the downstream effects of p53 inactivation, those of its homolog, p73, have yet to be elucidated. Therefore, I explore the transcriptional regulatory activity of p73 with two central hypotheses: 1) that p73 activates signaling pathways that drive stem cell differentiation upon genomic stability; and 2) that p73 deficient stem cells lack the ability to differentiate into mature adipocytes, proposing p73 as a crucial transcription factor in stem cell differentiation, specifically in the process of adipogenesis. Qualitative and quantitative analysis of differences in expression of mesenchymal stem cell (MSC) markers throughout the stages of adipogenesis between wild type (WT) induced pluripotent stem cells (iPSCs) and p73 knock-out (p73KO) iPSCs will provide insight into these hypotheses. Completion of these studies will enhance our understanding of the role of p73 in cellular maturation and will highlight the importance of tumor suppressor activity in preserving the integrity of the human genome.