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  • member
  • team
  • department
  • center
  • program_project
  • nrc
  • whocc
  • project
  • software
  • tool
  • patent
  • Administrative Staff
  • Assistant Professor
  • Associate Professor
  • Clinical Research Assistant
  • Clinical Research Nurse
  • Clinician Researcher
  • Department Manager
  • Dual-education Student
  • Full Professor
  • Honorary Professor
  • Lab assistant
  • Master Student
  • Non-permanent Researcher
  • Nursing Staff
  • Permanent Researcher
  • Pharmacist
  • PhD Student
  • Physician
  • Post-doc
  • Prize
  • Project Manager
  • Research Associate
  • Research Engineer
  • Retired scientist
  • Technician
  • Undergraduate Student
  • Veterinary
  • Visiting Scientist
  • Deputy Director of Center
  • Deputy Director of Department
  • Deputy Director of National Reference Center
  • Deputy Head of Facility
  • Director of Center
  • Director of Department
  • Director of Institute
  • Director of National Reference Center
  • Group Leader
  • Head of Facility
  • Head of Operations
  • Head of Structure
  • Honorary President of the Departement
  • Labex Coordinator
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← Go to Research

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Starting Date
24
May 2016
Status
Ongoing
Members
2
Structures
3
Publications
5

About

The maintenance of genome integrity plays a key role in the regeneration potential of stem cells, which are responsible for the homeostasis and regeneration of the tissue throughout life. DNA double strand breaks (DSBs) are extremely dangerous DNA lesions, which are generated by endogenous processes such as respiration and DNA replication, and exogenous treatments such as irradiation. DNA damage repair maintains genome integrity, and its impairment may affect cell or organism survival, or promote deleterious and cancer-initiating mutations. In adult stem cells impaired DSB repair may deplete the stem cell pool, induce anticipated differentiation, affect the entire progeny, and thereby impair tissue regeneration.

 In the lab, it has been shown that muscle stem cells (satellite cells) repair radiation-induced DSBs more efficiently and accurately than their committed progeny but the underlying mechanism is still unclear. DSB repair efficiency thus appears to decrease as a function of cell differentiation. We are currently investigating the mechanism by which satellite cells repair DSBs. We also study the contribution of specific DSB repair factors in maintaining the proliferation and differentiation potential of muscle stem cells.

References