GPR56 Is Essential for Testis Development and Male Fertility in Mice

被引:43
作者
Chen, Guangchun
Yang, Liquan
Begum, Shahinoor [2 ,3 ]
Xu, Lei [1 ]
机构
[1] Univ Rochester, Dept Biomed Genet, Dept Dermatol, Med Ctr, Rochester, NY 14642 USA
[2] MIT, Howard Hughes Med Inst, Cambridge, MA USA
[3] MIT, Koch Inst Integrat Canc Res, Cambridge, MA 02139 USA
关键词
GPR56; testis; seminiferous tubules; fertility; polarity; PROTEIN-COUPLED-RECEPTOR; SERTOLI-CELL DIFFERENTIATION; PERITUBULAR MYOID CELLS; BASEMENT-MEMBRANE; SEMINIFEROUS TUBULES; CHONDROITIN SULFATE; SEXUAL DEVELOPMENT; MAMMALIAN GONAD; CORD FORMATION; MOUSE TESTIS;
D O I
10.1002/dvdy.22468
中图分类号
R602 [外科病理学、解剖学]; R32 [人体形态学];
学科分类号
100101 ;
摘要
Testis development is critical for male fertility and continuation of the mammalian species. Essential structural components of testes are seminiferous tubules, which are lined by Sertoli cells and provide nutrients and physical protection for the maturation of sperm. Seminiferous tubule formation is initiated in embryos as testis cords and relies on their remodeling for maturation during development. Recently, three-dimensional image analyses showed that testis cords in different parts of embryonic gonads undergo distinct remodeling processes. How this asymmetric remodeling is regulated has not been investigated. We report here that the absence of an adhesion G protein-coupled receptor, GPR56, leads to partial disruption of seminiferous tubules and reduced fertility in male mice. The defects appear to originate asymmetrically in embryonic gonads, but subsequent to the initial establishment of testis cords, suggesting that GPR56 might act to establish a spatial and/or temporal cue for asymmetric cord remodeling during male gonad development. Developmental Dynamics 239:3358-3367, 2010. (C) 2010 Wiley-Liss, Inc.
引用
收藏
页码:3358 / 3367
页数:10
相关论文
共 57 条
  • [1] Morphogenesis of epithelial tubes: Insights into tube formation, elongation, and elaboration
    Andrew, Deborah J.
    Ewald, Andrew J.
    [J]. DEVELOPMENTAL BIOLOGY, 2010, 341 (01) : 34 - 55
  • [2] Homozygous inactivation of Sox9 causes complete XY sex reversal in mice
    Barrionuevo, F
    Bagheri-Fam, S
    Klattig, J
    Kist, R
    Taketo, MM
    Englert, C
    Scherer, G
    [J]. BIOLOGY OF REPRODUCTION, 2006, 74 (01) : 195 - 201
  • [3] MULLERIAN-INHIBITING SUBSTANCE FUNCTION DURING MAMMALIAN SEXUAL DEVELOPMENT
    BEHRINGER, RR
    FINEGOLD, MJ
    CATE, RL
    [J]. CELL, 1994, 79 (03) : 415 - 425
  • [4] Sertoli cell signaling by Desert hedgehog regulates the male germline
    Bitgood, MJ
    Shen, LY
    McMahon, AP
    [J]. CURRENT BIOLOGY, 1996, 6 (03) : 298 - 304
  • [5] Pdgfr-α mediates testis cord organization and fetal Leydig cell development in the XY gonad
    Brennan, J
    Tilmann, C
    Capel, B
    [J]. GENES & DEVELOPMENT, 2003, 17 (06) : 800 - 810
  • [6] One tissue, two fates: Molecular genetic events that underlie testis versus ovary development
    Brennan, J
    Capel, B
    [J]. NATURE REVIEWS GENETICS, 2004, 5 (07) : 509 - 521
  • [7] From cells to organs: building polarized tissue
    Bryant, David M.
    Mostov, Keith E.
    [J]. NATURE REVIEWS MOLECULAR CELL BIOLOGY, 2008, 9 (11) : 887 - 901
  • [8] BUEHR M, 1993, DEVELOPMENT, V117, P273
  • [9] The battle of the sexes
    Capel, B
    [J]. MECHANISMS OF DEVELOPMENT, 2000, 92 (01) : 89 - 103
  • [10] Desert hedgehog (Dhh) gene is required in the mouse testis for formation of adult-type Leydig cells and normal development of peritubular cells and seminiferous tubules
    Clark, AM
    Garland, KK
    Russell, LD
    [J]. BIOLOGY OF REPRODUCTION, 2000, 63 (06) : 1825 - 1838