Kenneth H. Albrecht, Ph.D.

Kenn Albrecht, Ph.D.
Assistant Professor of Medicine
Assistant Professor of Genetics and Genomics
Director of Transgenic Core Facility
Boston University School of Medicine
Post-doctoral Fellow, The Jackson Laboratory
1993 Ph.D. Genetics, The University of Connecticut
1986 B.S. Biology, SUNY Stony Brook
Other Appointments
Associate Director
BU Genome Science Institute
Graduate Program Affiliations
Cell and Molecular Biology
Genetics and Genomics
Molecular Medicine


Research Interests                                                                                                                                                                                        

xx_80 xyp_80 sprr_80 sry-egfp_80 sox9_80 pdgrfa_80

Mammalian gonadal sex determination is a powerful system for studying organogenesis, cell fate determination, and the evolution of sex chromosomes and developmental regulatory mechanisms. Besides basic scientific interest, mammalian sex determination also is of biomedical interest. Approximately one in 1000 infants has a gonadal or genital anomaly. Furthermore, many of the known genes involved in sex determination also are implicated in pathological processes such as tumorigenesis and primary adrenal failure, and have essential roles in the normal development of organs other than the gonads. We use the mouse as a model system for studying mammalian sex determination and gonad organogenesis and employ genetic, molecular genetic, genomic, cell biological and embryological techniques.

In mammals, XY fetuses develop testes due to the action of the Y-linked testis determining gene Sry (sex-determining region, Y chromosome) and XX fetuses develop ovaries in its absence. SRY is a DNA binding protein, and is likely a transcription factor that regulates other genes in the sex determination pathway. The mammalian gonadal precursors (the genital ridges) are bipotential and capable of differentiating as either testes or ovaries. It is generally accepted that each genital ridge contains a complete set of lineage precursors that are capable of adopting an ovarian or testicular cell-type fate. This “common precursor” hypothesis is best viewed as a series of bipotential cell fate decisions within the four cell lineages that comprise the gonad: germ cells, connective tissue cells, steroid producing cells and supporting cells. The current model proposes that Sry expression in the genital ridge initiates testis development by directing supporting cell precursors to develop as Sertoli rather than granulosa cells and that the development of all other gonadal cell types is dependent on the differentiation of the supporting cell lineage. Besides Sertoli cell differentiation, two direct consequences of Sry expression are the initiation of a male specific pattern of cell proliferation and the induction of mesenchymal cell migration from the adjacent mesonephros into the developing testis, a process necessary for testis cord development.

Although it is clear that expression of Sry is the trigger for testis differentiation, the molecular mechanisms of Sry function remain an enigma. For example, no downstream SRY target genes have been unequivocally identified and the regulation of Sry expression remains largely unexplored. A number of genes involved in gonadogenesis and sex determination have been identified and characterized; however, the position and relationship of these genes within the pathway remain to be defined and many more genes remain to be discovered. For example, most of the identified genes are transcription factors and not effector molecules. Additionally, our understanding of the genes involved in ovary development is particularly thin. Our future studies will include investigating the regulation of Sry expression, defining the position and relationship of known genes and identifying new genes in the gonad differentiation and sex determination pathways, and exploring basic mechanisms of gonad differentiation.

Selected Publications

Pazin, DE and Albrecht, KH. 2009. Developmental expression of Smoc1 and Smoc2 suggests potential roles in fetal gonad and reproductive tract differentiation.
Dev Dyn: in press.

Lee HJ, Pazin DE, Kahlon RS, Correa SM, Albrecht KH. 2009. Novel markers of early ovarian pre-granulosa cells are expressed in an Sry-like pattern. Dev Dyn 238: 812-825.

Liu P, Pazin DE, Merson RR, Albrecht KH, Vaziri C. 2009. The developmentally-regulated Smoc2 gene Is repressed by Aryl-hydrocarbon receptor (Ahr) signaling.Gene 433: 72-80.

Izvolsky KI, Lu J, Martin G, Albrecht KH, Cardoso WV. 2008. Systemic inactivation of Hs6st1 in mice is associated with late postnatal mortality without major defects in organogenesis. genesis 46:8-18.

Liu L, Brown D, McKee M, LeBrasseur NK, Yang D, Albrecht KH, Ravid K, Pilch PF. 2008. Deletion of Cavin/PTRF causes global loss of caveolae, dyslipidemia, and glucose intolerance. Cell Metabolism 8:310-317.

Bouma GJ, Washburn LL, Albrecht KH, Eicher EM. 2007. Correct dosage of Fog2 and Gata4 transcription factors is critical for fetal testis development in mice. PNAS 104:14994-14999.

Dewing P, Chiang CW, Sinchak K, Sim H, Fernagut PO, Kelly S, Chesselet MF, Micevych PE, Albrecht KH, Harley VR, Vilain E. 2006. Direct regulation of adult brain function by the male-specific factor SRY. Curr Biol 16:415-420.

Bouma GJ, Albrecht KH, Washburn LL, Recknagel AK, Churchill GA and Eicher EM. 2005. Gonadal sex reversal in mutant Dax1 XY mice: a failure to up-regulate Sox9 in pre-Sertoli cells. Development 132:3045-3054.

Thevenet L, Albrecht KH, Malki S, Berta P, Boizet-Bonhoure B, Poulat F. 2005. NHERF/SIP-1 interacts with mouse SRY via a different mechanism than human SRY. J Biol Chem 280:38625-38630.

Albrecht KH, Young M, Washburn LL, and Eicher EM. 2003. Sry expression level and protein isoform differences play a role in abnormal testis development in C57BL/6J mice carrying certain Sry alleles. Genetics 164: 277-288.

Tevosian SG, Albrecht KH, Crispino JD, Fujiwara Y, Eicher EM, and Orkin SH. 2002. Gonadal differentiation, sex determination and normal Sry expression require direct interaction between transcription partners GATA4 and FOG2. Development 129: 4627-4634.

Washburn LL, Albrecht KH, and Eicher EM. 2001. C57BL/6J-T-associated sex reversal in mice is caused by reduced expression of a Mus domesticus Sry allele. Genetics 158:1675-1681.

Albrecht KH and Eicher EM. 2001. Evidence that Sry is expressed in pre-Sertoli cells and Sertoli and granulosa cells share a common precursor. Dev Biol 240:92-107. (Featured as cover image).

Albrecht KH, Capel B, Washburn LL, and Eicher EM. 2000. Defective mesonephric cell migration is associated with abnormal testis cord development in C57BL/6J XYMus domesticus mice. Dev Biol 225:26-36.

Bergstrom DE, Young M, Albrecht KH, and Eicher EM. 2000. Related function of mouse SOX3, SOX9, and SRY HMG domains assayed by male sex determination. genesis 28:111-124.

Capel B, Albrecht KH, Washburn LL, and Eicher EM. 1999. Migration of mesonephric cells into the mammalian gonad depends on Sry. Mech Dev 84:127-131.

Albrecht KH, Oswald C, Brooks N, and Krider HM. 1991. An analysis of abnormal oocyte, daughterless-abo-like and wavoid in Drosophila: Related genes that affect ovaries and embryos. Biol Bull 181(3): 5

Albrecht KH and Eicher EM. 1997. DNA sequence analysis of Sry alleles (subgenus Mus) implicates misregulation as the cause of C57BL/6J YPOS sex reversal and defines the SRY functional unit. Genetics 147:1267-1277.

Laufer H and Albrecht KH. 1990. Metabolism of methyl farnesoate by peripheral tissues of the spider crab, Libinia emarginata. In: Advances in Invertebrate Reproduction 5, Hoshi M, Yamashita O (eds.). Elsevier, Amsterdam, 217-2

Albrecht KH and Laufer H. 1989. The metabolism of methyl farnesoate in Libinia emarginata. Biol Bull 176(1):6.


Albrecht KH and Eicher EM. 2002. Sex determination, mouse. In: Encyclopedia of Genetics, Brenner S, Miller JH (eds.). Academic Press, New York, pp. 1816-181.

Albrecht KH and Eicher EM. 2002. Mouse sex-reversed rearrangement. In: Encyclopedia of Genetics, Brenner S, Miller JH (eds.). Academic Press, New York, pp. 1253-12