PAR-3 defines a central subdomain of the cortical actin cap in mouse eggsDuncan FE, et al .
The evolutionarily conserved partitioning defective (PAR) protein PAR-3 is pivotal for establishing and maintaining cell polarity. During mammalian oocyte maturation, the radially symmetric oocyte is transformed into a highly polarized metaphase II (MII)-arrested egg. We therefore examined several aspects of PAR-3 expression during oocyte maturation. We cloned two novel PAR-3 transcripts from an oocyte library that likely encode proteins of M(r) = 73 K and 133 K that are phosphorylated during maturation. PAR-3, which is found throughout the GV-intact oocyte, becomes asymmetrically localized during meiosis. Following germinal vesicle breakdown, PAR-3 surrounds the condensing chromosomes and associates with the meiotic spindles. Prior to emission of the first and second polar bodies, PAR-3 is located within a central subdomain of the polarized actin cap, which overlies the spindle. This cortical PAR-3 localization depends on intact microfilaments. These results suggest a role for PAR-3 in establishing asymmetry in the egg and in defining the future site of polar body emission.
NCBI Summary:
This gene encodes a cell surface glycoprotein and member of the immunoglobulin superfamily of proteins. The encoded protein is involved in cell adhesion and cell communication in numerous cell types, but particularly in cells of the immune and nervous systems. The encoded protein is widely used as a marker for hematopoietic stem cells. This gene may function as a tumor suppressor in nasopharyngeal carcinoma. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Jul 2015]
General function
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Cellular localization
Nuclear
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Ovarian function
Oocyte maturation, Early embryo development
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Expression regulated by
FSH
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Ovarian localization
Oocyte, Theca
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CD90 and CD105 expression in the mouse ovary and testis at different stages of postnatal development. Tepekoy F et al. (2015) CD90 (i.e., THY1) and CD105 (i.e., endoglin) are glycoproteins known as mesenchymal stem cell markers that are expressed in various cell types including male and female gonadal cells. We aimed to determine ovarian and testicular expression of CD90 and CD105 in various cell types during postnatal development in mice. The present study was carried out on male (C57BL/6) and female (Balb/C) mice during critical stages of gonadal development. Immunohistochemical localization of CD90 and CD105 was determined in the ovaries obtained at postnatal days (PND) -1, -7, -21 and -60 and in the testes obtained at PND6, -8, -16, -20, -29, -32 and -88. The relative expression of CD90 and CD105 was evaluated by ImageJ software and data were analyzed by analysis of variance. The relative expression of CD90 and CD105 varied during postnatal development and increased significantly in the adult ovary (PND60) and testis (PND88) compared to the early postnatal gonads. In the ovaries, the expression of CD90 was significantly higher in somatic cells in comparison to germ cell compartments. In the testis, CD90 expression was greater in germ cells and Sertoli cells compared to other cell types. Expression of CD105 was higher in germ cells than somatic cells of both the ovary and testis. In addition to different expression of CD90 and CD105 during various developmental stages, also their altered expression in particular cell types suggests specific roles of these glycoproteins in physiological processes of mouse gonads.//////////////////
PMID: 26679159 The Roles of THY1 and Integrin Beta3 in Cell Adhesion During Theca Cell Layer Formation and the Effect of Follicle-Stimulating Hormone on THY1 and Integrin Beta3 Localization In Mouse Ovarian Follicles. Itami S et al. The mechanism of theca cell layer formation in mammalian ovaries has not been elucidated. In the present study, we examined the roles of THY1 and integrin beta3 in theca cell layer formation during mouse folliculogenesis. The localization pattern of THY1 and integrin beta3 in adult mouse ovary was immunohistochemically investigated. The strongest THY1 signal was observed in theca cell layers from secondary to preantral follicles, at which time theca cells have begun to participate in follicle formation. Integrin beta3 also localized to the theca cell layer of secondary to preantral follicles and showed a localization pattern that was similar to that of THY1. Moreover, the role of THY1 in theca cell layer formation was examined using a follicle culture system. When anti-THY1 antibody was added to this culture, no theca cell layers were formed and the granulosa cells were distanced from each other. Since a THY1 signal was not observed in ovaries at stages earlier than prepuberty, THY1 localization also appeared to be affected by mouse development. This possibility was examined by determination of the effect of administration of follicle-stimulating hormone, luteinizing hormone and 17beta-estradiol to 7-day-old mice on THY1 localization in the ovary 3 days later. Only follicle-stimulating hormone induced a THY1 signal in 10-day-old mouse ovaries. No THY1 signal was observed in untreated 10-day-old ovaries. In conclusion, THY1 might play a role in cell adhesion via binding to integrin beta3 in mouse ovaries. Our results suggest that THY1 localization may be affected by follicle-stimulating hormone in mouse ovaries.