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Mol. Hum. Reprod. Advance Access originally published online on February 15, 2006
Molecular Human Reproduction 2006 12(3):145-149; doi:10.1093/molehr/gal017
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© The Author 2006. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

An investigation into FOXE1 polyalanine tract length in premature ovarian failure

Wendy J. Watkins1, Sarah E. Harris2, Megan J. Craven1, Andrea L. Vincent3, Ingrid M. Winship4, Ksenija Gersak5 and Andrew N. Shelling1,6

1Department of Obstetrics and Gynaecology, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand, 2Department of Psychology, University of Edinburgh, Edinburgh, UK, 3Department of Ophthalmology, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand, 4Genetic Health Services, Royal Children’s Hospital, Parkville, Victoria, Australia and 5Department of Obstetrics and Gynaecology, University Medical Centre, Ljubljana, Slovenia

6 To whom correspondence should be addressed at: Department of Obstetrics and Gynaecology, Faculty of Medical and Health Sciences, Private Bag 92019, University of Auckland, Auckland, New Zealand. Email: a.shelling{at}auckland.ac.nz

Premature ovarian failure (POF) is a common condition affecting 1% of women worldwide. There is strong evidence for genetic involvement in POF as many cases are familial, and mutations in several genes have been associated with POF. We investigated variation in FOXE1 polyalanine tract length, following the observation that polyalanine tract deletions are seen in the closely related FOXL2 in patients with POF. In addition, polyalanine tract expansions in FOXL2 are often seen in patients with blepharophimosis–ptosis–epicanthus inversus syndrome (BPES), a rare eyelid disorder often associated with POF. The FOXE1 polyalanine tract shows marked variation in its length between POF patients and normal controls, existing as an allele of 12, 14, 16, 17 or 19 alanine residues. We found evidence to suggest that variation in FOXE1 polyalanine tract length predisposes to POF.

Key words: blepharophimosis–ptosis–epicanthus inversus syndrome/forkhead/FOXE1/polyalanine tract/premature ovarian failure


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