Portrait of Dr Peter Ellis

Dr Peter Ellis

Senior Lecturer in Molecular Genetics and Reproduction

About

Dr Peter Ellis is a Lecturer in Molecular Genetics and Reproduction at the University of Kent. Key findings from his work to date include the identification of novel genes on the mouse Y chromosome that affect sperm head shape and fertility; the discovery of a genomic conflict or arms race between the X and Y chromosomes in mice as they compete to influence offspring sex ratio, which in turn has dramatically affected the structural and functional content of both chromosomes; and the identification of mechanisms regulating meiotic and post-meiotic transcriptional silencing of the sex chromosomes. His laboratory investigates the molecular biology of reproduction, the conflicting roles played by sex-linked genes in regulating this process, and the relationship between DNA damage repair mechanisms and the checkpoints governing meiotic progression. Qualifications: 

  • MA in Medical Sciences, University of Cambridge (1999) 
  • PhD, University of Cambridge (2004) 
  • PGCHE and FHEA (2016) 

https://orcid.org/0000-0001-9709-

Research interests

DNA damage repair in reproduction and cancer
Meiotic germ cells and cancer cells share a number of unusual features including the activation of specific genes (the cancer-testis antigens), the ability to tolerate high numbers of DNA strand breaks without undergoing apoptosis, and (in oocytes) a lowered stringency spindle assembly checkpoint that permits cell division even in the presence of unattached kinetochores. Dr Ellis studies the intracellular mechanisms that monitor DNA damage and chromosomal alignment during cell division in order to understand how these are perturbed in disease states. 

The role of Yq-linked genes in fertility and offspring sex ratio
Mouse chromosome arm Yq is highly ampliconic, with Yq-linked genes being present in up to ~600 copies. Deletions on Yq (Yqdel) titrate the copy number level of the ampliconic genes on this chromosome arm. Yqdel males show a dose-dependent fertility phenotype, with smaller deletions leading to mild teratozoospermia and larger deletions leading to severe teratozoospermia and infertility. In the fertile males with smaller deletions, there is an offspring sex ratio skew in favour of females. Since X and Yqdel-bearing sperm are produced in equal numbers, the skew must be due to differential fertilising capacity between X-bearing and Yqdel-bearing sperm. Dr Ellis’ work in this model system is aimed at clarifying the physiological basis of the sex ratio skew, and understanding the molecular functions of the Yq-encoded genes that regulate sex ratio. 

Mechanisms of non-Mendelian inheritance
The earliest genetic concept taught in schools is Mendel’s First Law of Segregation: that you have two copies of each gene, and an equal chance of passing on either of the copies. Dr Ellis studies how and why Mendel’s Law breaks down, allowing meiotic drive genes – so-called genetic outlaws – to bias the reproductive lottery and promote their own inheritance. Key questions to resolve are how many driving genes there are, where they are in the genome, and how they work. 

Teaching

Dr Ellis teaches on a wide range of undergraduate and postgraduate courses

  • Genetics and Evolution - BI324 
  • The Genome - BI549  (from Spring 2019/20, module convenor) 
  • Research Project - BI600  
  • Integrated Endocrinology and Metabolism - BI626  
  • The Science of Reproductive Medicine - BI841 
  • MSc Project - BI845  (module convenor) 
  • Landscapes of the Future - PO681  (guest seminar)  

Supervision

MSc-R projects available for 2021

Understanding the engine of evolution (MSc Research by Genetics)

Jointly supervised by Marta Farre Belmonte

All genetic variation ultimately stems from the introduction of new mutations during gametogenesis. While the mutational processes operating in tumorigenesis are beginning to be unravelled, leading to the known COSMIC mutational signatures, those operating in the germline are much less well characterised.  In this bioinformatics project, we will take advantage of the recent availability of several high quality genomes from different mouse species to identify mutations specific to lab mouse using comparative genomics methods.

Comparison with existing data sets will then allow identification of the types of mutations associated with meiotic strand breaks, overall recombinational hotspots, spermatid-specific strand breaks occurring during sperm maturation, and oxidative damage incurred by mature sperm. This will allow us to develop a comprehensive all-round overview of the mutational pressures during male gametogenesis and how this relates to the rates of evolutionary change in different parts of the genome.

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