Dr David Miller

Reader in Molecular Andrology

0113 343 7804

Summary: Molecular and genetic aspects of male infertility and reproductive function.

Location: Division of Reproduction and Early Development

Teaching Commitments: MSc Clinical Embryology: Module leader for Module 1 in Fundamentals of Clinical Embryology and Module 6 Research Proposal. MSc Lifestyle, Ageing and Reproductive Health: Programme manager and module leader of Module 1 (Fundamentals of Clinical embryology-1), Module 2 (Fundamentals of Clinical embryology-2) and Research Module. Module in Molecular Human Reproduction for intercalated BSc in Clinical Sciences



BSc (Glasgow), PhD (Liverpool), PGCE (Canterbury)

Research Area

My group is interested in the underlying causes of male factor infertility and reproductive disfunction, the great majority of which, has unknown causes. Using wholly non-invasive methods that make use of ejaculate spermatozoa, we are compiling an RNA database that describes the fertile male and comparing this with RNA profiles obtained from the semen of infertile men. In this way, we aim to identify gene expression pathways that are affected in the infertile male. At the same time, if we know what RNAs are present in the spermatozoon, we can identify, by comparison with the RNAs that are present in the egg, those that are specific to and delivered by the sperm. Once we have identified these 'male' specific messages, we can begin assessing whether they have any function or influence on the developing embryo.

In a similar vein, we are looking more closely at how chromatin is packaged in the spermatozoon. So far we have found that DNA in human and murine sprermatozoa is packaged by a mixture of histones (as is the case with all somatic cells) and protamines (peculiar to spermatozoa). More interestingly, we have important evidence that different regions of the DNA are differentially packaged into these two compartments such that genic regions are enriched in the histone bound regions. This has important implications for male fertility because it suggests that some important stretches of DNA in sperm chromatin, containing particular gene sequences may be more susceptible to intrinsic or externally regulated damage, leading to sperm dysfunction. See Saida et al, 2011 and Arapanhi et al, 2009.