Home
/
Data resources
/
Literature
/
18509161
Lim homeobox gene, lhx8, is essential for mouse oocyte differentiation and survival.

Biol Reprod, 2008/9;79(3):442-9.

Choi Y[1], Ballow DJ, Xin Y, Rajkovic A

Affiliations

PMID: 18509161DOI: 10.1095/biolreprod.108.069393

Impact factor: 4.161

Abstract
Lhx8 is a member of the LIM-homeobox transcription factor family and preferentially expressed in oocytes and germ cells within the mouse ovary. We discovered that Lhx8 knockout females lose oocytes within 7 days after birth. At the time of birth, histological examination shows that Lhx8-deficient (Lhx8-/-) ovaries are grossly similar to the newborn wild-type ovaries. Lhx8-/- ovaries fail to maintain the primordial follicles, and the transition from primordial to growing follicles does not occur. Lhx8-/- ovaries misexpress oocyte-specific genes, such as Gdf9, Pou5f1, and Nobox. Very rapid loss of oocytes may partly be due to the drastic downregulation of Kit and Kitl in Lhx8-/- ovaries. We compared Lhx8-/- and wild-type ovaries using an Affymetrix 430 2.0 microarray platform. A total of 80 (44%) of 180 of the genes downregulated more than 5-fold in Lhx8-/- ovaries were preferentially expressed in oocytes, whereas only 3 (2%) of 146 genes upregulated more than 5-fold in the absence of Lhx8 were preferentially expressed in oocytes. In addition, the comparison of genes regulated in Lhx8-/- and Nobox-/- newborn ovaries discovered a common set of 34 genes whose expression level was affected in both Lhx8- and Nobox-deficient mice. Our findings show that Lhx8 is a critical factor for maintenance and differentiation of the oocyte during early oogenesis, and it acts in part by downregulating the Nobox pathway.
MeSH terms
Animals; Animals, Newborn; Cell Differentiation; Cell Survival; Embryo, Mammalian; Female; Gene Expression Regulation, Developmental; Gonads; Homeodomain Proteins; LIM-Homeodomain Proteins; Male; Meiosis; Mice; Mice, Inbred C57BL; Mice, Transgenic; Oocytes; Oogenesis; Signal Transduction; Transcription Factors
More resources
EndNote: Download