Dr Diane Rebourcet

Dr Diane Rebourcet

Postdoctoral Research Associate

Office PVC - Science

Career Summary

Biography

After attending fascinating lectures in Life Sciences, while undertaking my undergraduate studies at Paris-Denis-Diderot University, France, I decided to specialise in Reproduction and Development and completed a Masters degree in that same institution. I then began a PhD focussing on the impact of environmental endocrine disruptors on the reproductive system at Lyon-Claude-Bernard University, France. In 2011, thanks to a fellowship from the Servier Institute (a non-profit association), I obtained funding to pursue my postdoctoral studies at the University of Edinburgh in the Centre for Reproductive Health, and in 2018, I was recruited by the University of Newcastle as a Postdoctoral Research Associate.

Research expertise

My work includes a variety of subjects that reflect my research interests from when I first graduated to present day. From an early start in biological sciences, I carried out research in the area of reproduction, mainly focusing on reproductive pathologies and starting with the female reproductive system in relation with ovarian disorders (PCOS and premature ovarian failure). During my postgraduate studies, I felt especially pertained by the impact and consequences of the environment on human health, and therefore, extended my research interests to reproductive toxicology and endocrine disruption. Undertaking my PhD and first postdoctoral position in this field, I had the opportunity to address the impact of endocrine disruption on the male reproductive system development and function. My current research focuses on understanding the mechanisms and regulations affecting the reproductive system, amongst which the androgen biosynthesis (mainly undertaken by the Leydig cells) and in developing new approaches for potential therapies to benefit male health.

Current aspects of research:

  • The recent identification of new roles for Sertoli cells has fundamentally changed our understanding of testis biology regarding its development and function. My research interest is to pursue the characterisation of Sertoli cell roles and to utilise their properties as biological therapeutical tools.
  • Demonstrating the complexity of Sertoli cell regulation of Leydig cell development and function, Sertoli cells appear as a novel target for endocrine disruption and/or potential therapy to improve androgen profile. One focus on my ongoing research is to identify Sertoli cell factors that can regulate Leydig cells function,
  • With the recent identification of differential androgens pathways (classical and backdoor), another aspect of my ongoing research focuses on deciphering the importance of both classical and backdoor androgen pathways on testis development and function.
  • With a better understanding of androgen regulation, finding targeted and suitable therapies is another topic of my current research.

Common approaches: transgenic mouse models, “gene therapy”, biotechnologies, in silico modelling as well as usual bio-molecular techniques.

Teaching expertise

I have lectured for the University of Edinburgh in the Reproductive Systems (BIME10016) Undergraduate 4th year Course since 2014. I had the opportunity during my position in Edinburgh to be involved in the day-to-day supervision of PhD students and to supervise laboratory projects for both Bachelor of Science (Reproductive Biology) and Master of Science (Reproductive Science) students, both of which graduated with distinction.

Collaborations

I am working in close collaboration with world leading researchers: Peter O’Shaughnessy (University of Glasgow), Rod Mitchell (University of Edinburgh), Serge Nef (University of Geneva), Peter Stanton and Liza O’Donnell (Hudson Institute of Medical Research).


If you are a prospective Honours/PhD student and interested in joining the laboratory, please contact me via email: diane.rebourcet@newcastle.edu.au



Qualifications

  • PhD (Reproductive Biology), Claude Bernard University Lyon 1, France
  • Master in Cellular Biology Physiology & Pathology, Claude Bernard University Lyon 1, France

Keywords

  • Biotechnology
  • Endocrine disruptors
  • Endocrinology
  • Fertility
  • Infertility
  • Reproductive Biology
  • Reproductive Sciences

Languages

  • French (Mother)
  • English (Fluent)

Fields of Research

Code Description Percentage
060803 Animal Developmental and Reproductive Biology 45
060699 Physiology not elsewhere classified 15
110306 Endocrinology 40

Professional Experience

UON Appointment

Title Organisation / Department

Academic appointment

Dates Title Organisation / Department
15/6/2011 - 17/6/2012 Post-doctorate researcher University of Edinburgh
Medical Research Council (MRC) Centre for Reproductive Health
United Kingdom
18/6/2012 - 19/6/2015 Post-doctorate researcher University of Edinburgh
Medical Research Council (MRC) Centre for Reproductive Health
United Kingdom
17/6/2015 - 31/3/2018 Postdoctoral Research fellow University of Edinburgh
Medical Research Council (MRC) Centre for Reproductive Health
United Kingdom

Invitations

Keynote Speaker

Year Title / Rationale
2018 Effect of Sertoli cell ablation on testicular development and function.
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Publications

For publications that are currently unpublished or in-press, details are shown in italics.


Chapter (1 outputs)

Year Citation Altmetrics Link
2018 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]
DOI 10.1007/978-1-4939-7698-0_15
Citations Scopus - 3
Co-authors Annalucia Darbey, Lee Smith

Journal article (20 outputs)

Year Citation Altmetrics Link
2020 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, 34 10373-10386 (2020) [C1]
DOI 10.1096/fj.202000361R
Co-authors Lee Smith, Annalucia Darbey
2019 Rebourcet D, Monteiro A, Cruickshanks L, Jeffery N, Smith S, Milne L, et al., 'Relationship of transcriptional markers to Leydig cell number in the mouse testis', PloS one, 14 (2019) [C1]
DOI 10.1371/journal.pone.0219524
Citations Scopus - 1Web of Science - 1
Co-authors Lee Smith
2019 Gannon A-L, O'Hara L, Mason JI, Rebourcet D, Smith S, Traveres A, et al., 'Ablation of glucocorticoid receptor in the hindbrain of the mouse provides a novel model to investigate stress disorders', SCIENTIFIC REPORTS, 9 (2019) [C1]
DOI 10.1038/s41598-019-39867-y
Citations Scopus - 2Web of Science - 2
Co-authors Lee Smith, Annelouise Gannon
2019 Rebourcet D, O'Shaughnessy PJ, Smith LB, 'The expanded roles of Sertoli cells: lessons from Sertoli cell ablation models', Current Opinion in Endocrine and Metabolic Research, 6 42-48 (2019) [C1]
DOI 10.1016/j.coemr.2019.04.003
Co-authors Lee Smith
2018 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]
DOI 10.1038/s41598-018-30011-w
Citations Scopus - 4Web of Science - 5
Co-authors Lee Smith, Annalucia Darbey
2017 van den Driesche S, Kilcoyne KR, Wagner I, Rebourcet D, Boyle A, Mitchell R, et al., 'Experimentally induced testicular dysgenesis syndrome originates in the masculinization programming window', JCI insight, 2 e91204 (2017)

The testicular dysgenesis syndrome (TDS) hypothesis, which proposes that common reproductive disorders of newborn and adult human males may have a common fetal origin, is largely ... [more]

The testicular dysgenesis syndrome (TDS) hypothesis, which proposes that common reproductive disorders of newborn and adult human males may have a common fetal origin, is largely untested. We tested this hypothesis using a rat model involving gestational exposure to dibutyl phthalate (DBP), which suppresses testosterone production by the fetal testis. We evaluated if induction of TDS via testosterone suppression is restricted to the "masculinization programming window" (MPW), as indicated by reduction in anogenital distance (AGD). We show that DBP suppresses fetal testosterone equally during and after the MPW, but only DBP exposure in the MPW causes reduced AGD, focal testicular dysgenesis, and TDS disorders (cryptorchidism, hypospadias, reduced adult testis size, and compensated adult Leydig cell failure). Focal testicular dysgenesis, reduced size of adult male reproductive organs, and TDS disorders and their severity were all strongly associated with reduced AGD. We related our findings to human TDS cases by demonstrating similar focal dysgenetic changes in testes of men with preinvasive germ cell neoplasia (GCNIS) and in testes of DBP-MPW animals. If our results are translatable to humans, they suggest that identification of potential causes of human TDS disorders should focus on exposures during a human MPW equivalent, especially if negatively associated with offspring AGD.

DOI 10.1172/jci.insight.91204
Citations Scopus - 37Web of Science - 38
2017 Soffientini U, Rebourcet D, Abel MH, Lee S, Hamilton G, Fowler PA, et al., 'Identification of Sertoli cell-specific transcripts in the mouse testis and the role of FSH and androgen in the control of Sertoli cell activity', BMC GENOMICS, 18 (2017) [C1]
DOI 10.1186/s12864-017-4357-3
Citations Scopus - 8Web of Science - 7
Co-authors Lee Smith
2017 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]
DOI 10.1210/en.2017-00196
Citations Scopus - 36Web of Science - 29
Co-authors Annalucia Darbey, Lee Smith
2017 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]
DOI 10.1038/s41598-017-09016-4
Citations Scopus - 14Web of Science - 12
Co-authors Lee Smith, Annalucia Darbey, Annelouise Gannon
2016 Rebourcet LB, Wu J, Cruickshanks L, Smith SE, Milne L, Fernando A, et al., 'Sertoli cells modulate testicular vascular network development, structure, and function to influence circulating testosterone concentrations in adult male mice', Endocrinology, 157 2479-2488 (2016) [C1]
DOI 10.1210/en.2016-1156
Citations Scopus - 20Web of Science - 13
Co-authors Lee Smith
2015 Guillermet-Guibert J, Smith LB, Halet G, Whitehead MA, Pearce W, Rebourcet D, et al., 'Novel Role for p110 beta PI 3-Kinase in Male Fertility through Regulation of Androgen Receptor Activity in Sertoli Cells', PLOS GENETICS, 11 (2015) [C1]
DOI 10.1371/journal.pgen.1005304
Citations Scopus - 17Web of Science - 19
Co-authors Lee Smith
2015 Smith LB, O'Shaughnessy PJ, Rebourcet D, 'Cell-specific ablation in the testis: what have we learned?', ANDROLOGY, 3 1035-1049 (2015) [C1]
DOI 10.1111/andr.12107
Citations Scopus - 28Web of Science - 22
Co-authors Lee Smith
2014 Rebourcet D, O'Shaughnessy PJ, Pitetti J-L, Monteiro A, O'Hara L, Milne L, et al., 'Sertoli cells control peritubular myoid cell fate and support adult Leydig cell development in the prepubertal testis', DEVELOPMENT, 141 2139-2149 (2014) [C1]
DOI 10.1242/dev.107029
Citations Scopus - 64Web of Science - 57
Co-authors Lee Smith
2014 Rebourcet D, O'Shaughnessy PJ, Monteiro A, Milne L, Cruickshanks L, Jeffrey N, et al., 'Sertoli Cells Maintain Leydig Cell Number and Peritubular Myoid Cell Activity in the Adult Mouse Testis', PLOS ONE, 9 (2014) [C1]
DOI 10.1371/journal.pone.0105687
Citations Scopus - 60Web of Science - 47
Co-authors Lee Smith
2013 Halperin J, Devi YS, Elizur S, Stocco C, Shehu A, Rebourcet D, et al., 'Prolactin Signaling through the Short Form of Its Receptor Represses Forkhead Transcription Factor FOXO3 and Its Target Gene galt Causing a Severe Ovarian Defect (vol 22, pg 513, 2008)', MOLECULAR ENDOCRINOLOGY, 27 1981-1981 (2013)
2012 Magre S, Rebourcet D, Ishaq M, Wargnier R, Debard C, Meugnier E, et al., 'Gender differences in transcriptional signature of developing rat testes and ovaries following embryonic exposure to 2,3,7,8-TCDD', PLoS ONE, 7 (2012)

Dioxins are persistent organic pollutants interfering with endocrine systems and causing reproductive and developmental disorders. The objective of our project was to determine th... [more]

Dioxins are persistent organic pollutants interfering with endocrine systems and causing reproductive and developmental disorders. The objective of our project was to determine the impact of an in utero exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on reproductive function of male and female offspring in the rat with a special emphasis on the immature period. We used a low dose of TCDD (unique exposure by oral gavage of 200 ng/kg at 15.5 days of gestation) in order to mirror a response to an environmental dose of TCDD not altering fertility of the progeny. We choose a global gene expression approach using Affymetrix microarray analysis, and testes of 5 days and ovaries of 14 days of age. Less than 1% of the expressed genes in gonads were altered following embryonic TCDD exposure; specifically, 113 genes in ovaries and 56 in testes with 7 genes common to both sex gonads. It included the repressor of the aryl hydrocarbon receptor (Ahrr), the chemokines Ccl5 and Cxcl4 previously shown to be regulated by dioxin in testis, Pgds2/Hpgds and 3 others uncharacterized. To validate and extend the microarray data we realized real-time PCR on gonads at various developmental periods of interest (from 3 to 25 days for ovaries, from 5 to the adult age for testes). Overall, our results evidenced that both sex gonads responded differently to TCDD exposure. For example, we observed induction of the canonic battery of TCDD-induced genes coding enzymes of the detoxifying machinery in ovaries aged of 3-14 days of age (except Cyp1a1 induced at 3-10 days) but not in testes of 5 days (except Ahrr). We also illustrated that inflammatory pathway is one pathway activated by TCDD in gonads. Finally, we identified several new genes targeted by TCDD including Fgf13 in testis and one gene, Ptgds2/Hpgds regulated in the two sex gonads. © 2012 Magre et al.

DOI 10.1371/journal.pone.0040306
Citations Scopus - 13Web of Science - 12
2011 Naville D, Rebourcet D, Chauvin MA, Vega N, Jalabert A, Vigier M, et al., 'Direct and indirect impact of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on adult mouse Leydig cells: An in vitro study', Toxicology Letters, 207 251-257 (2011)

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and related substances are ubiquitous environmental pollutants that exert adverse effects on reproductive processes. In testis, Leydig c... [more]

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and related substances are ubiquitous environmental pollutants that exert adverse effects on reproductive processes. In testis, Leydig cells which produce testosterone are under hormonal and local control exerted by cytokines including TNFa. Using mouse Leydig primary cell cultures as a model, we studied the effects of TCDD on the steroidogenic outcome of Leydig cells and the gene expression levels of Ccl5 and Cxcl4, previously shown to be target genes of TCDD in testis. We found that TCDD did not alter the steroidogenic outcome of Leydig cells but that it up-regulated Cxcl4 gene expression levels. TCDD also impacted Ccl5 gene expression when cells had been co-treated with TNFa. TCDD action probably initiated with binding to the aryl hydrocarbon receptor (AhR) present on Leydig cells. TCDD regulated the gene expression levels of AhR (transient down-regulation) and its repressor AhRR and Cyp1b1 (up-regulation). The trophic human chorionic gonadotropin (hCG) hormone did not impact AhR, its repressor AhRR or Cyp1b1 but it opposed the TCDD-enhanced AhRR mRNA levels. Conversely, TNFa stimulated AhR gene expression levels. Collectively, it is suggested that the impact of TCDD on expression of target genes in Leydig cells may operate under the complex network of hormones and cytokines. © 2011 Elsevier Ireland Ltd.

DOI 10.1016/j.toxlet.2011.09.019
Citations Scopus - 14Web of Science - 9
2010 Rebourcet D, Odet F, Vérot A, Combe E, Meugnier E, Pesenti S, et al., 'The effects of an in utero exposure to 2,3,7,8-tetrachloro-dibenzo-p-dioxin on male reproductive function: Identification of Ccl5 as a potential marker', International Journal of Andrology, 33 413-424 (2010)

2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and dioxin-like compounds are widely encountered toxic substances suspected of interfering with the endocrine systems of humans and wild... [more]

2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and dioxin-like compounds are widely encountered toxic substances suspected of interfering with the endocrine systems of humans and wildlife, and of contributing to the loss of fertility. In this study, we determined the changes in testicular gene expression caused by in utero exposure to TCDD along with the intra-testicular testosterone levels, epididymal sperm reserves, daily sperm production (DSP) and testis histology. To this purpose, female pregnant Sprague-Dawley rats orally received TCDD (10, 100 or 200 ng/kg body weight) or vehicle at embryonic day 15, and the offspring was killed throughout development. Hepatic Cyp1a1 gene expression was measured in the offspring to confirm the exposure to TCDD. The gross histology of the testes and intra-testicular testosterone levels were normal among the studied groups. Sperm reserves were altered in 67-day-old rats of the TCDD-200 group, but not in 145-day-old animals or in the other TCDD-exposed groups. Nonetheless, fertility was not altered in males of the TCDD-200 group, and the F2 males generated had normal sperm reserves and DSP. Microarray analysis permitted the identification of eight differentially expressed genes in the 4-week-old testes of the TCDD-200 compared with that of the control group (cut-off value ± 1.40), including the down-regulated chemokine Ccl5/Rantes. Inhibition of Ccl5/Rantes gene expression was observed throughout development in the TCDD-200 group, and at 67 and 145 days in the TCDD-100 group (animals of younger ages were not examined). Ccl5/Rantes gene expression was mostly confined in Leydig cells. F2 males generated from males of the TCDD-200 group had normal levels of Ccl5/Rantes in testis and Cyp1a1 in liver, which might indicate that Ccl5/Rantes is a marker of TCDD exposure in testis such as Cyp1a1 in liver. In conclusion, we demonstrated a decrease in Ccl5/Rantes RNA levels and a transitory decline in sperm reserves in the testes of rats of TCDD-dosed dams. © 2010 European Academy of Andrology.

DOI 10.1111/j.1365-2605.2009.01020.x
Citations Scopus - 20Web of Science - 18
2010 Bachelot A, Bouilly J, Liu Y, Rebourcet D, Leux C, Kuttenn F, et al., 'Sequence variation analysis of the prolactin receptor C-terminal region in women with premature ovarian failure', FERTILITY AND STERILITY, 94 2772-2775 (2010)
DOI 10.1016/j.fertnstert.2010.06.040
Citations Scopus - 5Web of Science - 3
2008 Halperin J, Devi SY, Elizur S, Stocco C, Shehu A, Rebourcet D, et al., 'Prolactin signaling through the short form of its receptor represses forkhead transcription factor FOXO3 and its target gene galt causing a severe ovarian defect', MOLECULAR ENDOCRINOLOGY, 22 513-522 (2008)
DOI 10.1210/me.2007-0399
Citations Scopus - 36Web of Science - 39
Show 17 more journal articles

Conference (3 outputs)

Year Citation Altmetrics Link
2014 van den Driesche S, Rebourcet D, Kilcoyne K, Sharpe RM, 'Fetal Androgen Suppression in the Masculinisation Programming Window (MPW) Determines Adult Reproductive Disorders in the Rat', ENDOCRINE REVIEWS (2014)
2011 Naville D, Rebourcet D, Chauvin M, Vega N, Jalabert A, Vigier M, et al., 'Impact of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in adult mouse Leydig cells: An in vitro study', TOXICOLOGY LETTERS, Paris, FRANCE (2011)
DOI 10.1016/j.toxlet.2011.05.155
2011 Magre S, Rebourcet D, Ishaq M, Wargnier R, Debard C, Vidal H, et al., 'Alterations in the transcriptome of the developing ovaries and testes following embryonic exposure to 2,3,7,8-TCDD', TOXICOLOGY LETTERS, Paris, FRANCE (2011)
DOI 10.1016/j.toxlet.2011.05.849
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Grants and Funding

Summary

Number of grants 7
Total funding $616,487

Click on a grant title below to expand the full details for that specific grant.


20192 grants / $543,193

The Importance of Classical Versus Backdoor Androgen Production Pathways in Masculinisation, Fertility and Lifelong Male Health$519,443

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Professor Lee Smith, Doctor Diane Rebourcet
Scheme Project Grant
Role Investigator
Funding Start 2019
Funding Finish 2021
GNo G1800098
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON Y

Investigating the regulation of androgen production to support healthy male ageing across the life course$23,750

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Diane Rebourcet, Doctor Elizabeth Bromfield, Dr Curley Michael
Scheme Research Grant
Role Lead
Funding Start 2019
Funding Finish 2020
GNo G1901563
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

20161 grants / $1,000

Society For Endocrinology travel grant $1,000

Funding body: Society For Endocrinology

Funding body Society For Endocrinology
Project Team

Dr Diane Rebourcet

Scheme SFE-Travel grant
Role Lead
Funding Start 2016
Funding Finish 2016
GNo
Type Of Funding External
Category EXTE
UON N

20151 grants / $18,000

Determining the Testicular Interstitial Fluid Proteome: Identification of Sertoli cell-derived paracrine factors regulating lifelong Leydig cell function.$18,000

Funding body: Society For Endocrinology

Funding body Society For Endocrinology
Project Team

Dr Diane Rebourcet (CIA), Prof Lee Smith, Dr Peter Stanton, Dr Liza O'Donnell

Scheme SFE-Early Career Grant
Role Lead
Funding Start 2015
Funding Finish 2015
GNo
Type Of Funding External
Category EXTE
UON N

20121 grants / $3,614

MSc Reproductive Science studentship, University of Edinburgh.$3,614

Funding body: MSc Reproductive Science studentship

Funding body MSc Reproductive Science studentship
Project Team

Dr Diane Rebourcet (PI), Annalucia Darbey (student)

Scheme MSc Reproductive Science studentship, University of Edinburgh.
Role Lead
Funding Start 2012
Funding Finish 2013
GNo
Type Of Funding Internal
Category INTE
UON N

20111 grants / $31,680

Timing and regulation of Sertoli cell proliferation in perinatal life and its vulnerability to disruption by lifestyle/environmental chemical exposures.$31,680

Funding body: Research funding from Servier Association

Funding body Research funding from Servier Association
Project Team

Dr Diane Rebourcet (CIA), Pr Richard Sharpe

Scheme Research funding
Role Lead
Funding Start 2011
Funding Finish 2012
GNo
Type Of Funding External
Category EXTE
UON N

20101 grants / $19,000

Effects of an in Utero Exposure to 2,3-7,8 TCDD on the rat reproductive system and role of the aryl hydrocarbon receptor in mouse testicular physiology.$19,000

Funding body: Schering-Plough research funds

Funding body Schering-Plough research funds
Project Team

Diane Rebourcet (CIA), Dr Brigitte Battistoni-Le Magueresse

Scheme Research funds
Role Investigator
Funding Start 2010
Funding Finish 2010
GNo
Type Of Funding External
Category EXTE
UON N
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Research Opportunities

Importance of the classical and backdoor androgen pathways in testis development and function.

PhD project

PHD

Faculty of Science

14/1/2019 - 15/6/2021

Contact

Doctor Diane Rebourcet
University of Newcastle
Office PVC - Science
diane.rebourcet@newcastle.edu.au

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Dr Diane Rebourcet

Position

Postdoctoral Research Associate
Lee Smith Group
Office PVC - Science
Faculty of Science

Contact Details

Email diane.rebourcet@newcastle.edu.au
Phone (02)491 38060
Fax (02) 49216308

Office

Room Life Sciences Building - LS2.02
Building Life Sciences Building
Location Callaghan
University Drive
Callaghan, NSW 2308
Australia
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