Colin E. Bishop Ph.D., Professor

SHORT BIOGRAPHIC SKETCH: Dr. Colin Bishop was born in Portsmouth, England. He received his Ph.D in Immunogenetics in 1979 from the Department of Immunology, London Hospital Medical College, University of London. After a postdoctoral fellowship at the Netherlands Cancer Institute, Amsterdam, he moved to the Institute Pasteur, Paris in 1981 where he worked on the genetics of sex-determination. In 1990 he moved to the University of Tennessee, Memphis where he was Professor in the Departments of Obstetrics & Gynecology and Microbiology & Immunology, and Director of basic research for the OB/GYN laboratories. In 1993 he returned to France to direct the INSERM (NIH equivalent) research unit 406 “Medical Genetics and Development” at the La Timone Hospital, Marseille. He was also a founding member of the “Developmental Biology Institute of Marseille-Luminy” (IBDM). After 3 years he returned to the USA to take up the position of Professor at Baylor College of Medicine, Houston in the Department of Obstetrics & Gynecology, with a joint appointment as Professor in the Department of Molecular & Human Genetics. He also directed the basic research program for OB/GYN Laboratories. He joined WFIRM in September 2006 and directs the genetics and developmental biology component of the Institute.

SYNOPSIS OF AREA OF INTEREST: Dr. Bishop’s research interests are focused on reproductive genetics. These include primary sex-determination, germ cell development, stem cell biology and human reproductive failure.

DETAILED AREA OF INTEREST: The overall focus concerns the genetics of primary sex determination, germ cell development and fertility. Two main themes are being developed. The first is concerned with the genetic basis of primary sex determination and germ cell development. In order to address this problem we are generating a national resource of new mouse strains, carrying mutations in genes affecting fertility and sex determination. This project which uses novel transposon technology can be seen at <http://mousegenome.bcm.tmc.edu/bartmice/>. We have now begun to analyze several selected new infertility mutants generated in this program. These involve XX female-to-male sex-reversal; male and/or female infertility, due to defects at specific stages of germ cell development; sperm-egg fusion and pre-implantation failure. All of these models were chosen as they closely mimic aspects of sex-reversal and human infertility conditions such as those seen in XX(Y-) sex reversal/gonadal dysgenesis, Sertoli Cell only syndrome, Premature Ovarian Failure, and failure of egg penetration. As such, they represent attractive animal models for investigating the regulation of these developmental processes and provide an important component in the generation of knowledge-based therapies. We have recently expanded this technology to modify the rat genome which is particularly relevant due to the fact that despite worldwide efforts, rat embryonic stem cells have not yet been produced.

The second main theme is the identification of genetic factors influencing stem cell renewal and differentiation during gametogenesis. We are particularly interested in deriving functional germ cells from adult-derived stem cells. Our long term goal is to be able to repopulate the testes or ovaries of infertile patients with germ cells derived from autologous tissue.

Reproductive genetics touches the very core of our existence – the ability of human beings to procreate. Developments in this field have led to legal and ethical issues which society has yet to resolve. Assisted reproductive technologies have forced society to re-examinE the current concept of the family, the right of every human to create life, and the rights of potential children and parents. It is obviously essential that we understand the basic biology underlying such developments at the most fundamental level. Equally important is that we fully appreciate and openly debate the ethical implications of such research.

PUBLICATIONS
Qin Y, Ling-Kun K, Poirier C, Truong C, Overbeek P and Bishop CE. (2004) Long-range activation of Sox9 in Odd Sex (Ods) mice. Hum. Mol. Genet. (2004) 13(12):1213-8.

Lorenzetti D, Bishop CE, Justice MJ. (2004) Deletion of the Parkin coregulated gene causes male sterility in the quakingviable mouse mutant. Proc. Natl. Acad. Sci. U S A. 101 8402-8407.

Rohozinski J and Bishop CE. (2004) The mouse juvenile spermatogonial depletion (jsd) phenotype is due to a mutation in the X-dereived retrogene Utp14b.
Proc. Natl. Acad Sci. U S A. 101 11695-11700

Qin Y and Bishop CE. (2005) Sox9 is sufficient for functional testis development producing fertile male mice in the absence of Sry. Hum. Mol. Genet. 14: 1221-1229

Aubin I, Adams CP, Opsahl S, Septier D, Bishop CE, Auge N, Salvayre R, Negre-Salvayre A, Goldberg M, Guenet JL, Poirier C. A (2005) Deletion in the gene encoding sphingomyelin phosphodiesterase 3 (Smpd3) results in osteogenesis and dentinogenesis imperfecta in the mouse. Nature Genetics 37:803-5.

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