Foxl2 disruption causes mouse ovarian failure by pervasive blockage of follicle development

FOXL2 mutations cause gonadal dysgenesis or premature ovarian failure (POF) in women, as well as eyelid/forehead dysmorphology in both sexes (the 'blepharophimosis-ptosis-epicanthus inversus syndrome', BPES). Here we report that mice lacking Foxl2 recapitulate relevant features of human BP...

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Published in:	Human molecular genetics Vol. 13; no. 11; p. 1171
Main Authors:	Uda, Manuela, Ottolenghi, Chris, Crisponi, Laura, Garcia, Jose Elias, Deiana, Manila, Kimber, Wendy, Forabosco, Antonino, Cao, Antonio, Schlessinger, David, Pilia, Giuseppe
Format:	Journal Article
Language:	English
Published:	England 01.06.2004
Subjects:	Animals Blepharophimosis - etiology Blepharophimosis - genetics Disease Models, Animal DNA-Binding Proteins - genetics DNA-Binding Proteins - physiology Embryo, Mammalian - pathology Eyelids - abnormalities Female Forkhead Box Protein L2 Forkhead Transcription Factors Gene Deletion Immunochemistry Ki-67 Antigen - immunology Male Mice Mice, Knockout Ovary - embryology Ovary - growth & development Ovary - pathology Primary Ovarian Insufficiency - etiology Primary Ovarian Insufficiency - genetics Primary Ovarian Insufficiency - pathology Syndrome Transcription Factors - genetics Transcription Factors - physiology
ISSN:	0964-6906
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Abstract	FOXL2 mutations cause gonadal dysgenesis or premature ovarian failure (POF) in women, as well as eyelid/forehead dysmorphology in both sexes (the 'blepharophimosis-ptosis-epicanthus inversus syndrome', BPES). Here we report that mice lacking Foxl2 recapitulate relevant features of human BPES: males and females are small and show distinctive craniofacial morphology with upper eyelids absent. Furthermore, in mice as in humans, sterility is confined to females. Features of Foxl2 null animals point toward a new mechanism of POF, with all major somatic cell lineages failing to develop around growing oocytes from the time of primordial follicle formation. Foxl2 disruption thus provides a model for histogenesis and reproductive competence of the ovary.
AbstractList	FOXL2 mutations cause gonadal dysgenesis or premature ovarian failure (POF) in women, as well as eyelid/forehead dysmorphology in both sexes (the 'blepharophimosis-ptosis-epicanthus inversus syndrome', BPES). Here we report that mice lacking Foxl2 recapitulate relevant features of human BPES: males and females are small and show distinctive craniofacial morphology with upper eyelids absent. Furthermore, in mice as in humans, sterility is confined to females. Features of Foxl2 null animals point toward a new mechanism of POF, with all major somatic cell lineages failing to develop around growing oocytes from the time of primordial follicle formation. Foxl2 disruption thus provides a model for histogenesis and reproductive competence of the ovary.FOXL2 mutations cause gonadal dysgenesis or premature ovarian failure (POF) in women, as well as eyelid/forehead dysmorphology in both sexes (the 'blepharophimosis-ptosis-epicanthus inversus syndrome', BPES). Here we report that mice lacking Foxl2 recapitulate relevant features of human BPES: males and females are small and show distinctive craniofacial morphology with upper eyelids absent. Furthermore, in mice as in humans, sterility is confined to females. Features of Foxl2 null animals point toward a new mechanism of POF, with all major somatic cell lineages failing to develop around growing oocytes from the time of primordial follicle formation. Foxl2 disruption thus provides a model for histogenesis and reproductive competence of the ovary. FOXL2 mutations cause gonadal dysgenesis or premature ovarian failure (POF) in women, as well as eyelid/forehead dysmorphology in both sexes (the 'blepharophimosis-ptosis-epicanthus inversus syndrome', BPES). Here we report that mice lacking Foxl2 recapitulate relevant features of human BPES: males and females are small and show distinctive craniofacial morphology with upper eyelids absent. Furthermore, in mice as in humans, sterility is confined to females. Features of Foxl2 null animals point toward a new mechanism of POF, with all major somatic cell lineages failing to develop around growing oocytes from the time of primordial follicle formation. Foxl2 disruption thus provides a model for histogenesis and reproductive competence of the ovary.
Author	Uda, Manuela Cao, Antonio Pilia, Giuseppe Deiana, Manila Crisponi, Laura Kimber, Wendy Garcia, Jose Elias Schlessinger, David Forabosco, Antonino Ottolenghi, Chris
Author_xml	– sequence: 1 givenname: Manuela surname: Uda fullname: Uda, Manuela organization: Laboratory of Genetics, National Institute on Aging, Baltimore, MD 21224, USA – sequence: 2 givenname: Chris surname: Ottolenghi fullname: Ottolenghi, Chris – sequence: 3 givenname: Laura surname: Crisponi fullname: Crisponi, Laura – sequence: 4 givenname: Jose Elias surname: Garcia fullname: Garcia, Jose Elias – sequence: 5 givenname: Manila surname: Deiana fullname: Deiana, Manila – sequence: 6 givenname: Wendy surname: Kimber fullname: Kimber, Wendy – sequence: 7 givenname: Antonino surname: Forabosco fullname: Forabosco, Antonino – sequence: 8 givenname: Antonio surname: Cao fullname: Cao, Antonio – sequence: 9 givenname: David surname: Schlessinger fullname: Schlessinger, David – sequence: 10 givenname: Giuseppe surname: Pilia fullname: Pilia, Giuseppe
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/15056605$$D View this record in MEDLINE/PubMed
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PublicationTitle	Human molecular genetics
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Snippet	FOXL2 mutations cause gonadal dysgenesis or premature ovarian failure (POF) in women, as well as eyelid/forehead dysmorphology in both sexes (the...
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SubjectTerms	Animals Blepharophimosis - etiology Blepharophimosis - genetics Disease Models, Animal DNA-Binding Proteins - genetics DNA-Binding Proteins - physiology Embryo, Mammalian - pathology Eyelids - abnormalities Female Forkhead Box Protein L2 Forkhead Transcription Factors Gene Deletion Immunochemistry Ki-67 Antigen - immunology Male Mice Mice, Knockout Ovary - embryology Ovary - growth & development Ovary - pathology Primary Ovarian Insufficiency - etiology Primary Ovarian Insufficiency - genetics Primary Ovarian Insufficiency - pathology Syndrome Transcription Factors - genetics Transcription Factors - physiology
Title	Foxl2 disruption causes mouse ovarian failure by pervasive blockage of follicle development
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