Deficiency of Reproductive Tract alpha (1,2)Fucosylated Glycans and Normal Fertility in Mice with Targeted Deletions of the FUT1 or FUT2 alpha (1,2)Fucosyltransferase Locus

doi:10.1128/MCB.21.24.8336-8345.2001

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Molecular and Cellular Biology, December 2001, p. 8336-8345, Vol. 21, No. 24
0270-7306/01/$04.00+0 DOI: 10.1128/MCB.21.24.8336-8345.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Deficiency of Reproductive Tract $alpha$ (1,2)Fucosylated Glycans and Normal Fertility in Mice with Targeted Deletions of the FUT1 or FUT2 $alpha$ (1,2)Fucosyltransferase Locus

Steven E. Domino,¹^,^* Liang Zhang,¹^, Patrick J. Gillespie,²^, Thomas L. Saunders,³ and John B. Lowe³^,⁴

Department of Obstetrics and Gynecology,¹ Department of Physiology,² Howard Hughes Medical Institute,³ and Department of Pathology,⁴ The University of Michigan Medical School, Ann Arbor, Michigan 48109

Received 31 August 2001/Accepted 10 September 2001

The fucose $alpha$ (1 $right-arrow$ 2) galactose $beta$ structure is expressed by uterine epithelial cells in the mouse and has been implicated in blastocystadhesion events thought to be required for murine implantation.Fuc $alpha$ (1 $right-arrow$ 2)Gal $beta$ moieties and cognate fucosyltransferases are alsoexpressed by epithelial cells of the male reproductive tract andhave been implicated in sperm maturation events that may contributeto fertilization. To determine directly if Fuc $alpha$ (1 $right-arrow$ 2)Gal $beta$ moietiesare required for fertility, we have generated strains of micethat are deficient in genes encoding FUT1 and FUT2, a pair ofGDP-L-fucose: $beta$ (1 $right-arrow$ 4)-D-galactosyl-R 2- $alpha$ -L-fucosyltransferase enzymes(EC 2.4.1.69) responsible for Fuc $alpha$ (1 $right-arrow$ 2)Gal $beta$ synthesis and expression.FUT1 null mice and FUT2 null mice develop normally and exhibitno gross phenotypic abnormalities. The Fuc $alpha$ (1 $right-arrow$ 2)Gal $beta$ epitope isabsent from the uterine epithelia of FUT2 null mice and from theepithelia of the epididymis of FUT1 null mice. Fully normal fertilityis observed in FUT1 null intercrosses and in FUT2 null intercrosses.These observations indicate that Fuc $alpha$ (1 $right-arrow$ 2)Gal $beta$ moieties are notessential to blastocyst-uterine epithelial cell interactions requiredfor implantation and are not required for sperm maturation eventsthat permit fertilization and that neither the FUT loci nor theircognate fucosylated glycans are essential to normaldevelopment.

^* Corresponding author. Mailing address: Department of Obstetrics and Gynecology, 6428 Medical Science Bldg. I, 1150 West MedicalCenter Dr., The University of Michigan, Ann Arbor, MI 48109-0617.Phone: (734) 647-9562. Fax: (734) 936-8617. E-mail: sedomino{at}med.umich.edu.

Present address: Henry Ford Hospital, Detroit, MI48202.

Present address: Pfizer Global Research & Development, Ann Arbor, MI48105.

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Deficiency of Reproductive Tract (1,2)Fucosylated Glycans and Normal Fertility in Mice with Targeted Deletions of the FUT1 or FUT2 (1,2)Fucosyltransferase Locus

Deficiency of Reproductive Tract $alpha$ (1,2)Fucosylated Glycans and Normal Fertility in Mice with Targeted Deletions of the FUT1 or FUT2 $alpha$ (1,2)Fucosyltransferase Locus