Dr Annalucia Darbey
Postdoctoral Research Associate
School of Environmental and Life Sciences
My first experience of research began at the University of Edinburgh where I undertook my degree in Masters in Research in Reproductive Sciences. During this time, I was afforded the opportunity to work under the supervision of Professor Lee Smith investigating the roles of Sertoli cells and using gene editing technologies such as Crispr/Cas9 for the study of Androgen Receptor.
I completed my PhD in 2018, continuing with Professor Lee Smith, as part of the Tissue Repair Programme at the University of Edinburgh. My PhD project was focussed upon the targeting and repair of adult testicular somatic cells through viral gene therapy. Following recruitment to The University of Newcastle as a Postdoctoral Research Associate in 2019, I now continue to investigate deliverable transgenics and their potential applications in the adult testis and wider endocrine systems. Development of this novel technology will permit the investigation of the genetics underpinning male fertility and androgen production and will lead to the development of novel bespoke therapeutics and contraceptives fulfilling a currently unmet need for millions of men worldwide.
Current Research Themes
My current research themes are focussed upon the development of novel technologies for both the investigation and the treatment of male reproductive disorders, including the investigation of alternative options for long lasting male contraceptives. To complement this, I am also investigating novel in vitro models of endocrine organs, which may prove vital for the investigation of new therapeutics in human cells. Therefore, I have a keen interest in deliverable transgenics, viral vectors, nanoparticle technology and 3D printing and biofabrication.
Whilst at the University of Edinburgh, I was involved in the teaching and supervision of undergraduate students; in particular on the Rebroductive Biology undergraduate course. This included the direct demonstration of techniques in practical lab sessions as well as supervision of tutorial groups through group assignments. Since being appointed at the University of Newcastle, I have lectured on Reproductive Physiology and Development Modules (BIOL3020) and supervised Biotechnology students on 3rd year placement projects.
- Doctor of Philosophy, University of Edinburgh - Scotland
- 3D Printing
- Deliverable Transgenics
- Gene Therapy
- Male Reproductive Biology
- Viral Vectors
- English (Mother)
Fields of Research
|100104||Genetically Modified Animals||25|
|Title||Organisation / Department|
For publications that are currently unpublished or in-press, details are shown in italics.
Chapter (1 outputs)
Rebourcet D, Darbey A, Curley M, O Shaughnessy P, Smith LB, 'Testicular cell selective ablation using diphtheria toxin receptor transgenic mice', Sertoli Cells: Methods and Protocols, Humana Press, New York, NY 203-228 (2018) [B1]
Journal article (5 outputs)
Rebourcet D, Mackay R, Darbey A, Curley MK, Jørgensen A, Frederiksen H, et al., 'Ablation of the canonical testosterone production pathway via knockout of the steroidogenic enzyme HSD17B3, reveals a novel mechanism of testicular testosterone production', FASEB journal : official publication of the Federation of American Societies for Experimental Biology, (2020)
© 2020 The Authors. The FASEB Journal published by Wiley Periodicals LLC on behalf of Federation of American Societies for Experimental Biology. Male development, fertility, and l... [more]
© 2020 The Authors. The FASEB Journal published by Wiley Periodicals LLC on behalf of Federation of American Societies for Experimental Biology. Male development, fertility, and lifelong health are all androgen-dependent. Approximately 95% of circulating testosterone is synthesized by the testis and the final step in this canonical pathway is controlled by the activity of the hydroxysteroid-dehydrogenase-17-beta-3 (HSD17B3). To determine the role of HSD17B3 in testosterone production and androgenization during male development and function we have characterized a mouse model lacking HSD17B3. The data reveal that developmental masculinization and fertility are normal in mutant males. Ablation of HSD17B3 inhibits hyperstimulation of testosterone production by hCG, although basal testosterone levels are maintained despite the absence of HSD17B3. Reintroduction of HSD17B3 via gene-delivery to Sertoli cells in adulthood partially rescues the adult phenotype, showing that, as in development, different cell-types in the testis are able to work together to produce testosterone. Together, these data show that HS17B3 acts as a rate-limiting-step for the maximum level of testosterone production by the testis but does not control basal testosterone production. Measurement of other enzymes able to convert androstenedione to testosterone identifies HSD17B12 as a candidate enzyme capable of driving basal testosterone production in the testis. Together, these findings expand our understanding of testosterone production in males.
Darbey A, Smith LB, 'Deliverable transgenics & gene therapy possibilities for the testes', Molecular and Cellular Endocrinology, 468 81-94 (2018) [C1]
Curley M, Milne L, Smith S, Atanassova N, Rebourcet D, Darbey A, et al., 'Leukemia Inhibitory Factor-Receptor is Dispensable for Prenatal Testis Development but is Required in Sertoli cells for Normal Spermatogenesis in Mice', SCIENTIFIC REPORTS, 8 (2018) [C1]
Rebourcet D, Darbey A, Monteiro A, Soffientini U, Tsai YT, Handel I, et al., 'Sertoli Cell Number Defines and Predicts Germ and Leydig Cell Population Sizes in the Adult Mouse Testis', ENDOCRINOLOGY, 158 2955-2969 (2017) [C1]
Patel SH, O'Hara L, Atanassova N, Smith SE, Curley MK, Rebourcet D, et al., 'Low-dose tamoxifen treatment in juvenile males has long-term adverse effects on the reproductive system: implications for inducible transgenics.', Scientific Reports, 7 (2017) [C1]
|Show 2 more journal articles|