Biomedical Science – Reproduction and Development

You should have or be expected to achieve, a minimum of a second class degree (2:2). For healthcare graduates, a pass is required. All degrees must be awarded before 1st August on the year of entry.

We welcome applications from individuals from a range of backgrounds, including humanities, science and healthcare.

We may invite you to interview if are unable to make a decision directly from your application. If you are invited for an interview you will be asked to write a short paper (no more than half a page) on a subject associated with biomedical research.

Alternative professional qualifications, or previous related experience, may be considered and we encourage you to apply.

We accept equivalent qualifications gained in other countries and use UKNARIC to assess. Please see our International Student Support pages for more information. If you have any questions, you can contact us at study@sgul.ac.uk

For details on English Language requirements, please see here. This is a Group 2 course.

You will be asked to outline your reasons for applying for the course in a brief personal statement on the application form. You will also need to provide two satisfactory references See the ‘Apply’ tab for more information.

This 30 credit module will begin with the exploration of the science of reproduction covering a range of aspects of women’s health including: normal sexual differentiation, endocrine disorders, hormonal control of fertility, pregnancy and contraception.

The module will also explore development and disease, covering embryonic development with an emphasis on molecular mechanisms and human congenital disorders. It will include an introduction to experimental techniques, terminology, model organisms and the use of transgenic mouse technology.

This pathway will take advantage of active reproduction and development research taking place at St George’s, laboratory skills sessions and clinical case-based lectures, giving you an insight into how understanding of the cellular processes involved in reproduction and development can help design strategies to aid fertility and treat/manage defects in development. The module will also provide you with insight into how new sequencing technologies and ‘omics’ methodologies are helping to decipher the cellular mechanisms involved in reproduction and development. 

The substantive research project is worth 105 credits. Here are some examples of past student projects.

Does oxygen regulate stanniocalcin-1 in pregnancy?

Aims: The aims of this project are: (1) to identify which cells within the placenta express STC-1; (2) to determine whether the secretion of STC-1 by the placenta and or trophoblasts are regulated by the concentration of oxygen; and (3) to determine whether STC-1 is elevated in the serum of women in the first trimester who later develop pre-eclampsia.

Brief overview: Stanniocalcin-1 (STC1) is a glycoprotein originally discovered in bony fish where it acts to regulate calcium and phosphate homeostasis. In mammals the protein has been implicated in a number of physiological and pathophysiological processes, including ovulation, lactation, organogenesis, cerebral ischemia and tumour angiogenesis. Although in humans it is expressed by a number of tissues it has only been reported in the serum of pregnancy women and is elevated in pregnancies complicated by pre-eclampsia. Pre-eclampsia is a disorder of pregnancy characterised in late gestation by endothelial cell dysfunction, high blood pressure and proteinuria. However, the origins are believed to be in the first trimester. It is a syndrome that affects up to 8 per cent of all pregnancies, resulting in poor placental perfusion and babies that are small for gestational age. The source of the STC-1 during pregnancy is not known and therefore the regulation of its secretion has not been studied.

Methods used for data collection: Tissue and cell culture, ELISA, western blot, immunohistochemistry.

The role of calcium signalling in ciliopathy induced retinal degeneration

Aims: To use zebrafish to investigate whether aberrant calcium signalling may underlie retinal degeneration in ciliopathy patients.

Brief Overview:  The cilium is a small antenna-like organelle located on the cell surface. It plays a major role in signalling pathways required for normal tissue development. There is an emerging group of human disorders, known as ciliopathies, which affect cilia function. The ciliopathies share many clinical features, including retinal degeneration leading to blindness. The photoreceptor (PR) has a modified cilium connecting the inner and outer segment, allowing transport of high-turnover light-sensitive opsins (including rhodopsin), synthesised within the cytoplasm, to the outer segment where they have their function. Cilia are enriched with ion channels required for activating the photo-transduction cascade through membrane depolarisation and stimulated neurotransmitter release. Indeed, PR death has been linked to PR overstimulation. Thus photoreceptor death might be linked to aberrant intracellular ion release. Using rhodopsin expression as readout of photoreceptor quantity, we performed an in situ hybridization (ISH) drug screen for modifiers of rhodopsin expression in zebrafish eyes using an ion channel ligand library. We found a number of calcium agonists and antagonists that affected rhodopsin gene expression. Using an eye-specific genetically encoded fluorescent calcium indicator, this project hopes to explore the function of PR cilia in relation to calcium release.

Methods used for data collection: Generation of transgenic zebrafish lines, confocal microscopy, morpholino gene knockdown, Immunohistochemistry, qPCR, zebrafish husbandry.

The effect of genome-engineered GNB1L mutations on WNT-signalling

Aims: 

1. Generate loss-of-function mutations of GNB1L and associated proteins in HEK-293 cells
2. Determine the effects of GNB1L inactivation on WNT-signalling in HEK-293 cells

Brief overview:  The GNB1L gene is commonly deleted in 22q11 Deletion Syndrome (22q11DS). 22q11DS results from hemizygous deletion of a region of chromosome 22q11.2. This leads to behavioural and psychiatric problems, including autism (ASD) and schizophrenia (SZ). The study of the molecular basis of 22q11DS therefore provides a valuable opportunity to gain greater understanding of common genetic factors that cause predisposition to both ASD and SZ. GNB1L has been independently associated with ASD and SZ. Patients with schizophrenia, but without 22q11 deletion, have altered levels of GNB1L within the pre-frontal cortex. Mice that are hemizygous for GNB1L display neuro-behavioural abnormalities associated with psychiatric diseases, including schizophrenia.

GNB1L has been linked to autism, following the identification of affected individuals and families with translocation/sequence variants involving this gene. Together, these data suggest that GNB1L may be involved in the pathogenesis of psychiatric illness in 22q11DS and in the wider population. Little is known about GNB1L function, but we have discovered that it is able to regulate the WNT-signalling pathway. WNT-signalling has been previously associated with ASD and SZ. This project will further explore the cellular function of GNB1L using genome engineering techniques to create inactivating mutations of GNB1L and associated proteins in cell culture. The student will then assess the effects of these mutations on WNT-signalling.

Methods used for data collection: Cell culture, transfection, SDS-PAGE, western blotting, immunofluorescence, reporter-assays, DNA cloning, CRISPR/Cas9 genome engineering, DNA sequencing.

Molecular pathogenesis of hypogonadotropic hypogonadism

Aims: Screening of genes involved in gonadal development using zebrafish model.

Brief Overview: Congenital idiopathic hypogonadotropic hypogonadism (CHH) refers to a failure to initiate or complete puberty naturally. CHH individuals are mostly infertile due to sex hormone (LH/FSH) deficiency. Kallmann syndrome (KS) is a type of CHH, but has the additional characteristic of an absent or abnormally decreased sense of smell, known as ‘anosmia’. KS/CHH can affect both men and women, and the current treatment is the administration of GnRH or gonadotrophin to induce puberty and restore fertility. However, a significant number of patients do not respond to the current treatment and never regain normal gonadal function.

The genetic basis of KS/CHH has been well documented and mutations of different genes have been identified in around 50 per cent of cases. This project aims to investigate the pathogenesis of CHH and KS using zebrafish as a model system. We will use targeted morpholino injections and CRISPR/Cas9 technology in zebrafish to validate the impact of KS/CHH gene knockdown in the normal sexual development and function of hypothalamus-pituitary-gonadal axis, ultimately revealing new insight in the mechanisms of KS/CHH.

Methods used for data collection: In situ hybridisation, immunohistochemistry, zebrafish embryo manipulation, PCR, microscope imaging.

During the first term you will meet potential supervisors to familiarise yourself with the research activity within each pathway and to identify an appropriate project. Broadly speaking, your topic should be within the fields of biomedical sciences, healthcare, or health services and use appropriate scientific methods.

The self-directed component of your course includes the in-depth study of an area of interest, developing research and presentation skills, and gaining insight into possible careers.

Teaching for core modules is concentrated in the autumn term. Teaching for specialist modules takes place over the year. Throughout this time you will either be attending lectures or laboratory sessions on most days of the week. Students choose their projects and start with laboratory work from mid-October, and complete their research by September.

Dissertation projects will involve the assembly, analysis and interpretation of data. Project titles and areas for research will be identified by module leaders and will relate to the pathway selected by the student.

Assessments are designed to help students with preparation for their dissertation. They help you review published work critically, use appropriate experimental design, and analyse experimental data. They also enable you to develop scientific writing and presentation skills.

All modules are assessed through written assignments or an oral presentation, with the exception of the statistics module which is assessed via examination. The optional modules require the submission of written reports. Following the research project, you will be asked to present a poster on your research.

1. Click the application link and create an account: Biomedical Science MRes - Reproduction and Development

2. Once you've created an account, you will then be able to complete an application form and upload any relevant documents. You can save a partly completed form and return to it later. Please make sure you complete all sections. Please make sure that the information you provide is accurate, including the options you select in menus.

3. Add pgadmissions@sgul.ac.uk to your address book to ensure you do not miss any important emails from us.

4. When you have checked that your application is complete and accurate, click ‘submit’.

You can track your application through your online account.

When completing your application, you will be asked to provide contact details of two referees. Please ensure these details are accurate. As soon as you have submitted your application, your referees will be contacted by the university asking them to upload a reference to your online application.

One must be a recent academic reference. The other should be either a second academic reference or a professional/employer reference. They should cover your suitability for the course and your academic ability.

Your referees should know you well enough, in an official capacity, to write about you and your suitability for higher education. We do not accept references from family, friends, partners, ex-partners or yourself.

We will send reminder emails to your referees but it is your responsibility to ensure that contact details are correct and referees are available to submit a reference. References should be uploaded within two weeks of making your application.