Dr Emilie Hollville

Dr Emilie Hollville
Dr Emilie Hollville
Dr Emilie Hollville

Lecturer

About
Email Address
emilie.hollville@abdn.ac.uk
Office Address
4.17 Institute of Medical Sciences
Foresterhill Campus
Ashgrove Road West
AB25 2ZD

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School/Department
School of Medicine, Medical Sciences and Nutrition

Biography

I graduated with honours in Cellular Biology and Physiology from the University of Versailles, France before receiving my PhD in Biochemistry, Molecular and Cellular Biology from the University of Paris-Saclay in 2009. Following my PhD, I obtained a postdoctoral research position at the Smurfit Institute of Genetics, Trinity College Dublin, Ireland. In 2015, I moved to North Carolina, USA to further gain experience in neuroscience, working as a postdoctoral research fellow at the Neuroscience Center of the University of North Carolina at Chapel Hill. I was appointed as a Lecturer at the University of Aberdeen in September 2022.

I have a particular interest in the role of programmed cell death, and more specifically a form of programmed cell death called apoptosis, in cell and tissue homeostasis. I have studied the regulation of the apoptotic machinery in various cellular models including cancer, development, and neurodegenerative disorders.

Qualifications

  • PhD Biochemistry, Molecular and Cellular Biology 
    2009 - Université Paris-Saclay, France 
  • MSc Cell Biology and Cancer Genetics 
    2004 - Université Paris-Saclay, France 
  • BSc Cellular Biology and Physiology 
    2003 - Université de Versailles Saint-Quentin en Yvelines, France 

Memberships and Affiliations

Internal Memberships

Institute of Medical Sciences, Equality, Diversity and Inclusion committee

School of Medicine, Medical Sciences and Nutrition, Laboratory Sustainability Working Group (LABSUS)

External Memberships

Member of the British Neuroscience Association (BNA)

Member of the Federation of European Neuroscience Societies (FENS)

Member of the ALBA Network

Research

Research Overview

Mechanisms controlling brain maturation and sustaining brain health throughout life


The postnatal programs that mature the nervous system are critical to refine neuronal circuits and connectivity for the emergence of individual behaviour. The genetic factors and pathways required for neuronal maturation (e.g. synaptic development and plasticity, neurite branching and arborization) are often found affected both in neurodevelopmental and neurodegenerative disorders.

My lab focuses on understanding the molecular and cellular pathways that support neuronal maturation and maintenance of lifelong neuronal health and survival. I am particularly interested in understanding the role played by ubiquitin ligases and programmed cell death regulators in these processes.

Arbor-spines reconstructions.png

Relevant publications

  • MicroRNA-29 is essential for brain maturation through regulation of CH methylation. Swahari V, Nakamura A, Hollville E, … , Anton ES, Greenberg ME, Deshmukh M. Cell Reports. 2021 Apr 6;35(1):108946. Link to publication
  • Apoptotic Cell Death Controls in Neurons. Hollville E, Romero S, Deshmukh M. FEBS J. 2019 Sep;286(17):3276-3298. Link to publication
  • Physiological functions of non-apoptotic caspase activity in the nervous system. Hollville E, Deshmukh M. Semin Cell Dev Biol. 2018 Oct;82:127-136. Link to publication

 

Mitochondrial quality control in neurodegenerative disorders


Age-related neurodegenerative disorders affect millions of people worldwide and are characterized by impairment in cognitive and/or motor functions. These disorders develop as a result of neuronal dysfunction in the brain or in the peripheral nervous system that eventually result in neuronal death. Common features of neurodegenerative disorders are mitochondrial function failure and defective clearance of damaged mitochondria.

Mitochondria are central hubs for metabolism, energy production, cytoplasmic calcium buffering, regulation of reactive oxygen species production and inflammation. High metabolic and calcium buffering activities, such as the ones required to sustain normal neuronal function, make mitochondria particularly prone to damage. Cells have developed a quality control mechanism for the targeted elimination of impaired mitochondria by autophagy, a process called mitophagy.

I am interested in understanding the interactions between neuronal activity and function and the mitochondrial quality control pathways.

Parkin-mediated mitophagy - Cell Rep 2014-2.png

Relevant publications

  • Characterization of a Cul9 – Parkin double knockout mouse model for Parkinson’s disease. Hollville E, Joers V, Nakamura A, Swahari V, Tansey MG, Moy SS, Deshmukh M. Scientific Reports. 2020 Oct 9;10(1):16886. Link to publication
  • Bcl-2 Family Proteins Participate in Mitochondrial Quality Control by Regulating Parkin/PINK1-Dependent Mitophagy. Hollville E, Carroll RG, Cullen SP, Martin SJ. Mol Cell. 2014 Aug 7;55(3):451-66. Link to publication
  • Parkin Sensitizes Towards Apoptosis Induced by Mitochondrial Depolarization Through Promoting Degradation of Mcl-1. Carroll RG, Hollville E, Martin SJ. Cell Reports. 2014 Nov 20; 9(4):1538–1553. Link to publication

Research Areas

Biomedical Sciences

Supervising

Research Specialisms

  • Molecular Biology
  • Cell Biology
  • Neuroscience
  • Biomedical Sciences

Our research specialisms are based on the Higher Education Classification of Subjects (HECoS) which is HESA open data, published under the Creative Commons Attribution 4.0 International licence.

Supervision

My current supervision areas are: Biomedical Sciences.

Supervisees

  • MX PAOLA MUSCOLINO
  • MS SANDRA MARIA SAJAN

Funding and Grants

The Royal Society Research Grant

UKRI BBSRC EASTBIO PhD Studentship 

Publications

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Contributions to Journals

Working Papers