Overview
Ellie obtained her BSc in Biology from the University of York in 2014. Subsequently, she joined the MRC-Asthma UK Centre in Allergic Mechanisms of Asthma at King’s College London, where she studied for an integrated MSc and PhD based around immunology and epigenetics. Her PhD project focused on DNA methylation in Helper T cells. After obtaining her PhD, Ellie worked in outreach, most recently working for the University of Exeter as an outreach officer. Ellie is currently working as a postdoctoral research assistant at the University of Exeter Medical School as part of the NIHR Exeter Biomedical Research Centre.
Qualifications
- PhD Immunology and Epigenetics, King’s College London
- MSc Immunology, King’s College London
- BSc(Hons) Biology, University of York
- PGCE (QTS), University of Exeter
Publications
Key publications | Publications by category | Publications by year
Publications by category
Journal articles
Callender LA, Schroth J, Carroll EC, Garrod-Ketchley C, Romano LEL, Hendy E, Kelly A, Lavender P, Akbar AN, Chapple JP, et al (2021). GATA3 induces mitochondrial biogenesis in primary human CD4+ T cells during DNA damage.
Nature Communications,
12(1).
Abstract:
GATA3 induces mitochondrial biogenesis in primary human CD4+ T cells during DNA damage
AbstractGATA3 is as a lineage-specific transcription factor that drives the differentiation of CD4+ T helper 2 (Th2) cells, but is also involved in a variety of processes such as immune regulation, proliferation and maintenance in other T cell and non-T cell lineages. Here we show a mechanism utilised by CD4+ T cells to increase mitochondrial mass in response to DNA damage through the actions of GATA3 and AMPK. Activated AMPK increases expression of PPARG coactivator 1 alpha (PPARGC1A or PGC1α protein) at the level of transcription and GATA3 at the level of translation, while DNA damage enhances expression of nuclear factor erythroid 2-related factor 2 (NFE2L2 or NRF2). PGC1α, GATA3 and NRF2 complex together with the ATR to promote mitochondrial biogenesis. These findings extend the pleotropic interactions of GATA3 and highlight the potential for GATA3-targeted cell manipulation for intervention in CD4+ T cell viability and function after DNA damage.
Abstract.
Lavender P, Kelly A, Hendy E, McErlean P (2018). CRISPR-based reagents to study the influence of the epigenome on gene expression.
Clinical and Experimental Immunology,
194(1), 9-16.
Abstract:
CRISPR-based reagents to study the influence of the epigenome on gene expression
Summary
. The use of epigenome editing is set to expand our knowledge of how epigenetic landscapes facilitate gene expression capacity within a given cell. As epigenetic landscape profiling in health and disease becomes more commonplace, so does the requirement to assess the functional impact that particular regulatory domains and DNA methylation profiles have upon gene expression capacity. That functional assessment is particularly pertinent when analysing epigenomes in disease states where the reversible nature of histone and DNA modification might yield plausible therapeutic targets. In this review we discuss first the nature of the epigenetic landscape, secondly the types of factors that deposit and erase the various modifications, consider how modifications transduce their signals, and lastly address current tools for experimental epigenome editing with particular emphasis on the immune system.
Abstract.
Publications by year
2021
Callender LA, Schroth J, Carroll EC, Garrod-Ketchley C, Romano LEL, Hendy E, Kelly A, Lavender P, Akbar AN, Chapple JP, et al (2021). GATA3 induces mitochondrial biogenesis in primary human CD4+ T cells during DNA damage.
Nature Communications,
12(1).
Abstract:
GATA3 induces mitochondrial biogenesis in primary human CD4+ T cells during DNA damage
AbstractGATA3 is as a lineage-specific transcription factor that drives the differentiation of CD4+ T helper 2 (Th2) cells, but is also involved in a variety of processes such as immune regulation, proliferation and maintenance in other T cell and non-T cell lineages. Here we show a mechanism utilised by CD4+ T cells to increase mitochondrial mass in response to DNA damage through the actions of GATA3 and AMPK. Activated AMPK increases expression of PPARG coactivator 1 alpha (PPARGC1A or PGC1α protein) at the level of transcription and GATA3 at the level of translation, while DNA damage enhances expression of nuclear factor erythroid 2-related factor 2 (NFE2L2 or NRF2). PGC1α, GATA3 and NRF2 complex together with the ATR to promote mitochondrial biogenesis. These findings extend the pleotropic interactions of GATA3 and highlight the potential for GATA3-targeted cell manipulation for intervention in CD4+ T cell viability and function after DNA damage.
Abstract.
2018
Lavender P, Kelly A, Hendy E, McErlean P (2018). CRISPR-based reagents to study the influence of the epigenome on gene expression.
Clinical and Experimental Immunology,
194(1), 9-16.
Abstract:
CRISPR-based reagents to study the influence of the epigenome on gene expression
Summary
. The use of epigenome editing is set to expand our knowledge of how epigenetic landscapes facilitate gene expression capacity within a given cell. As epigenetic landscape profiling in health and disease becomes more commonplace, so does the requirement to assess the functional impact that particular regulatory domains and DNA methylation profiles have upon gene expression capacity. That functional assessment is particularly pertinent when analysing epigenomes in disease states where the reversible nature of histone and DNA modification might yield plausible therapeutic targets. In this review we discuss first the nature of the epigenetic landscape, secondly the types of factors that deposit and erase the various modifications, consider how modifications transduce their signals, and lastly address current tools for experimental epigenome editing with particular emphasis on the immune system.
Abstract.
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