The differentiation of transplanted mammalian gonad primordia

Buyse, Adrian

doi:10.1002/jez.1400700102

Cited by 42 publications

(8 citation statements)

References 27 publications

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“…The mechanism of testicular organization in the absence of the Y chromosome remains Accepted February 19, 1993. Received December 17, 1992. In rats and mice, the XX gonadal primordium develops both testicular and ovarian structures (ovotestis) after transplantation into various sites of adult recipients [7][8][9][10][11][12][13][14]. We have previously reported that the mouse XX ovotestis contains ultrastructural characteristics of Sertoli cells [13,14].…”

Section: Introductionmentioning

confidence: 99%

Müllerian Inhibiting Substance Production Associated with Loss of Oocytes and Testicular Differentiation in the Transplanted Mouse XX Gonadal Primordium1

Taketo

Saeed

Manganaro

et al. 1993

Biology of Reproduction

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The mouse XX gonadal primordium develops seminiferous-like tubules after transplantation into the renal subcapsular site of the adult male or female mouse. We examined the ontogeny of Sertoli cell differentiation in XX gonadal grafts by immunocytochemical staining and organ culture bioassay for Müllerian Inhibiting Substance (MIS). During normal in situ development of the XY gonad, MIS staining was first detected in fetal Sertoli cells at 12 days of gestation (d.g.) and remained intense until 4 days postpartum (d.pp.), after which it gradually diminished with progressive testicular development. In the normal in situ XX gonad, MIS was detected in granulosa cells of growing follicles at 7 d.pp. and thereafter. When the XX gonad at 12 d.g. was grafted beneath the renal capsule, a few testicular cords composed of MIS-positive cells appeared on Day 7 post-transplantation (equivalent to 19 d.g.), much earlier than the normal appearance of MIS production in the intact XX ovary. The ovarian region containing germ cells at the meiotic prophase was unstained for MIS in the same sections. The incidence of XX gonadal grafts containing MIS-positive testicular cords and the number of such cords per gonadal graft steadily increased from Day 7 to Day 14 post-transplantation. Germ cells were absent or scarce inside the MIS-positive testicular cords. The MIS bioactivity in both control gonads and gonadal grafts coincided with the immunocytochemical staining for MIS. These results support the hypothesis that XX cells differentiate into Sertoli cells as a consequence of oocyte loss in the gonadal graft.

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Section: Introductionmentioning

confidence: 99%

Müllerian Inhibiting Substance Production Associated with Loss of Oocytes and Testicular Differentiation in the Transplanted Mouse XX Gonadal Primordium1

Taketo

Saeed

Manganaro

et al. 1993

Biology of Reproduction

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“…Seminiferous tubule-like structures have been observed in freemartin cattle (11), after premature oocyte death (12), and in XX gonads of W/W v mutant mice and busulphan-treated rats (13,14). They have also been observed in fetal rodent ovaries transplanted into male hosts (15) and aging rodents (16,17). The transdifferentiation of ovarian somatic cells to a testicular phenotype in these examples has been ascribed to the absence of viable oocytes (8,12) rather than the involvement of steroids.…”

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Estrogen regulates development of the somatic cell phenotype in the eutherian ovary

Britt¹,

Kerr²,

O’Donnell

et al. 2002

FASEB j.

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Steroids play a critical role in gonadal differentiation in birds, reptiles, and amphibia whereas gonadal differentiation in mammals is thought to be determined by genetic mechanisms. The gonads of female mice incapable of synthesizing estrogens due to disruption of the aromatase gene (ArKO) provide a unique model to test the role of estrogen in regulating the gonadal phenotype. We have shown that in the absence of estrogen, genetically female mice develop testicular tissue within their ovaries. The ovaries develop cells that possess structural and functional characteristics of testicular interstitial cells and of seminiferous tubule-like structures lined with Sertoli cells. Moreover, the ovaries express mRNA for the testis-specific Sertoli cell transcription factor Sox 9 and espin protein, which is specific for inter-Sertoli cell junctions. The development of the testicular tissue in this model can be reverted/postponed by replacing estrogen. When ArKO female mice were fed a diet containing phytoestrogens, the appearance of Leydig and Sertoli cells was postponed and reduced. Furthermore, administration of estradiol-17beta decreased the number of Sertoli and Leydig cells in the ovaries. These findings constitute definitive evidence that estrogen plays a critical role in maintaining female somatic interstitial and granulosa cells in the eutherian ovary.

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“…Before this stage, in a high percentage of cases, ovaries either do not develop at all or are prone to undergo spontaneous reversal, due apparently to incapacity of the prospective cortical component to develop effectively in abnormal tissue environments. On the other hand, the medullary component of the transplanted ovary suffers no such handicap and frequently assumes the lead in development (Buyse 1935, Moore & Price 1942, Holyoke 1949, Torrey 1950, Macintyre 1956, Macintyre et al 1960, Burns 1961, Bruner-Lorand 1964. When transplanted early in development, prospective ovaries may give rise to structures of four types: (1) poorly developed grafts of intermediate sex;…”

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“…(3) ovotestes in which both sex components are readily identifiable; (4) rudimentary testes (Buyse 1935, Macintyre et al 1960, Burns 1961, Bruner-Lorand 1964.…”

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Sex determination and gonadal differentiation in man

Boczkowski

1971

Clinical Genetics

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Sex determination in man and other mammals can be accounted for in terms of three postulates. First, that unless specifically inhibited, the differentiation of the primary gonads goes in the male direction. Second, that the specific inhibiting factor is produced by a structural gene probably located on the X chromosome; this gene need be expressed only in cells of the urogenital ridge. Third, this gene is “switched off” (rendered inactive) by a repressor substance produced by a structural gene located on the Y chromosome.

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The differentiation of transplanted mammalian gonad primordia

Cited by 42 publications

References 27 publications

Müllerian Inhibiting Substance Production Associated with Loss of Oocytes and Testicular Differentiation in the Transplanted Mouse XX Gonadal Primordium1

Müllerian Inhibiting Substance Production Associated with Loss of Oocytes and Testicular Differentiation in the Transplanted Mouse XX Gonadal Primordium1

Estrogen regulates development of the somatic cell phenotype in the eutherian ovary

Sex determination and gonadal differentiation in man

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