Delay of testicular differentiation in the B6.YDOM ovotestis demonstrated by immunocytochemical staining for Müllerian inhibiting substance

Taketo, Teruko; Saeed, Jamilah; Nishioka, Yasuhiko; Donahoe, Patricia K.

doi:10.1016/0012-1606(91)90240-4

Cited by 45 publications

(31 citation statements)

References 35 publications

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“…A mouse model for Klinefelter's syndrome (XXY) has recently been developed and tested for cognitive ability in a pavlovian learning task (Lue et al, 2005); XXY males mastered the task more slowly than did XY control males. In both experiments, the mice were gonad-intact at the time of testing and in both models, animals of the same gonadal sex are known to have different concentrations of steroid hormones during both development and adulthood (Taketo et al, 1991;Lue et al, 2005), which confounds the interpretation of these data. Using the same genetic cross used here but on a random bred MF1 background, we documented effects of gonadal sex on social preferences and masculine sexual behavior, but no effects of sex chromosome complement were found (De Vries et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Sex Chromosome Complement and Gonadal Sex Influence Aggressive and Parental Behaviors in Mice

Gatewood¹,

Wills²,

Shetty³

et al. 2006

J. Neurosci.

221

227

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Across human cultures and mammalian species, sex differences can be found in the expression of aggression and parental nurturing behaviors: males are typically more aggressive and less parental than females. These sex differences are primarily attributed to steroid hormone differences during development and/or adulthood, especially the higher levels of androgens experienced by males, which are caused ultimately by the presence of the testis-determining gene Sry on the Y chromosome. The potential for sex differences arising from the different complements of sex-linked genes in male and female cells has received little research attention. To directly test the hypothesis that social behaviors are influenced by differences in sex chromosome complement other than Sry, we used a transgenic mouse model in which gonadal sex and sex chromosome complement are uncoupled. We find that latency to exhibit aggression and one form of parental behavior, pup retrieval, can be influenced by both gonadal sex and sex chromosome complement. For both behaviors, females but not males with XX sex chromosomes differ from XY. We also measured vasopressin immunoreactivity in the lateral septum, which was higher in gonadal males than females, but also differed according to sex chromosome complement. These results imply that a gene(s) on the sex chromosomes (other than Sry) affects sex differences in brain and behavior. Identifying the specific X and/or Y genes involved will increase our understanding of normal and abnormal aggression and parental behavior, including behavioral abnormalities associated with mental illness.

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Section: Discussionmentioning

confidence: 99%

Sex Chromosome Complement and Gonadal Sex Influence Aggressive and Parental Behaviors in Mice

Gatewood¹,

Wills²,

Shetty³

et al. 2006

J. Neurosci.

221

227

View full text Add to dashboard Cite

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“…Moreover, Morris water maze learning performance has been reported to be more masculine in C57BL/6J XY POS female mice than in XX females (Stavnezer et al, 2000), although the fetal gonads of such females might contain some testicular tissue (Taketo et al, 1991), which could cause masculinization via a hormonal mechanism. These studies, together with the present findings, are consistent with a role for sex chromosome genes in neural and behavioral sexual differentiation.…”

Section: Discussionmentioning

confidence: 99%

A Model System for Study of Sex Chromosome Effects on Sexually Dimorphic Neural and Behavioral Traits

et al. 2002

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We tested the hypothesis that genes encoded on the sex chromosomes play a direct role in sexual differentiation of brain and behavior. We used mice in which the testis-determining gene (Sry) was moved from the Y chromosome to an autosome (by deletion of Sry from the Y and subsequent insertion of an Sry transgene onto an autosome), so that the determination of testis development occurred independently of the complement of X or Y chromosomes. We compared XX and XY mice with ovaries (females) and XX and XY mice with testes (males). These comparisons allowed us to assess the effect of sex chromosome complement (XX vs XY) independent of gonadal status (testes vs ovaries) on sexually dimorphic neural and behavioral phenotypes. The phenotypes included measures of male copulatory behavior, social exploration behavior, and sexually dimorphic neuroanatomical structures in the septum, hypothalamus, and lumbar spinal cord. Most of the sexually dimorphic phenotypes correlated with the presence of ovaries or testes and therefore reflect the hormonal output of the gonads. We found, however, that both male and female mice with XY sex chromosomes were more masculine than XX mice in the density of vasopressin-immunoreactive fibers in the lateral septum. Moreover, two male groups differing only in the form of their Sry gene showed differences in behavior. The results show that sex chromosome genes contribute directly to the development of a sex difference in the brain.

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“…It has been argued that the mechanism of testicular differentiation following loss of oocytes in the XX ovary may differ from that in the XY fetal testis [15]. XX Sertoli cell differentiation was demonstrated by immunocytochemical staining for MIS, which serves as an early and accurate marker of Sertoli cell differentiation in the XY gonad [16][17][18].…”

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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Delay of testicular differentiation in the B6.YDOM ovotestis demonstrated by immunocytochemical staining for Müllerian inhibiting substance

Cited by 45 publications

References 35 publications

Sex Chromosome Complement and Gonadal Sex Influence Aggressive and Parental Behaviors in Mice

Sex Chromosome Complement and Gonadal Sex Influence Aggressive and Parental Behaviors in Mice

A Model System for Study of Sex Chromosome Effects on Sexually Dimorphic Neural and Behavioral Traits

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

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