The pro-apoptotic gene Bax is required for the death of ectopic primordial germ cells during their migration in the mouse embryo

Stallock, James; Molyneaux, Kathy; Schaible, Kyle; Knudson, C. Michael; Wylie, Christopher

doi:10.1242/dev.00898

Cited by 123 publications

(118 citation statements)

References 28 publications

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“…It has long been known that the receptor tyrosine kinase Kit and its ligand stem cell factor regulate the migration, proliferation, and/or survival of PGCs (Mintz & Russell 1957, McCoshen & McCallion 1975, Buehr et al 1993, Gu et al 2009), presumably through the AKT/MTOR/BAX signaling pathway (De Miguel et al 2002, Stallock et al 2003, Runyan et al 2006. Similarly, mutations of RNA-binding proteins such as NANOS3, TIAL1, and DND1 have been known to lead to the loss of germ cells due to the failure of survival and/or proliferation of PGCs (Beck et al 1998, Tsuda et al 2003, Youngren et al 2005.…”

Section: Key Regulators For Pgc Specificationmentioning

confidence: 99%

Germ cell specification in mice: signaling, transcription regulation, and epigenetic consequences

Saitou¹,

Yamaji²

2010

Reproduction

127

117

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The specification of germ cell fate in development initiates mechanisms essential for the perpetuation of genetic information across the generations. Recent studies in mice have shown that germ cell specification requires at least three key molecular/cellular events: repression of the somatic program, re-acquisition of potential pluripotency, and an ensuing genome-wide epigenetic reprogramming. Moreover, a signaling and transcriptional principle governing these processes has been identified, raising the possibility of inducing the germ cell fate precisely from pluripotent stem cells in culture. These advances will in turn serve as a basis to explore the mechanism of germ cell specification in other mammals, including humans. The recapitulation of germ cell development in humans in culture will provide unprecedented opportunities to understand the basis of the propagation of our genome, both under normal and diseased conditions.

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Section: Key Regulators For Pgc Specificationmentioning

confidence: 99%

Germ cell specification in mice: signaling, transcription regulation, and epigenetic consequences

Saitou¹,

Yamaji²

2010

Reproduction

127

117

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“…These mislocalised germ cells can provide an undifferentiated germ cell substrate that can transform and establish extra-gonadal germ cell tumors. It has recently been shown that a key mechanism in eliminating these mis-localised germ cells is the down-regulation of SCF and the activation of intrinsic cell death that is mediated through the pro-apoptotic gene Bax (Stallock et al, 2003;Runyan et al, 2006). Finally, TGFβ1 and ACTIVIN limit PGC proliferation in various tissue culture systems (Godin and Wylie, 1991;Richards et al, 1999).…”

Section: Survival and Proliferation: Key Aspects Of Early Germ Cell Dmentioning

confidence: 99%

Foetal germ cells: striking the balance between pluripotency and differentiation

Western¹

2009

Int. J. Dev. Biol.

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“…Serum-free culture mimics a growth factor withdrawal situation. A protective effect of Bax deletion on oocyte viability following growth factor withdrawal has been demonstrated (De Felici et al 1999, Stallock et al 2003, suggesting that granulosa cells are similarly less susceptible to death following growth factor withdrawal in the absence of Bax.…”

Section: Discussionmentioning

confidence: 99%

BAX is involved in regulating follicular growth, but is dispensable for follicle atresia in adult mouse ovaries

Greenfeld¹,

Babus²,

Furth³

et al. 2007

Reproduction

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Mammalian females are endowed with a finite number of primordial follicles at birth or shortly thereafter. Immediately following the formation of the primordial follicle pool, cohorts of these follicles are recruited to begin growth, and this recruitment continues until the primordial follicle population is depleted. Once recruited, a follicle will either grow and ovulate or undergo atresia. Follicle atresia results from the apoptotic death of follicular cells. Members of the BCL-2 family of proteins are important regulators of apoptosis in most cells including in the ovary. Here, we tested the hypothesis that the proapoptotic BAX is an important regulator of follicle survival. We used a variety of histological and biochemical techniques to investigate the impact of Bax deletion on follicle growth and death. We observed that the Bax deletion results in delayed vaginal opening and altered follicular growth. Young adult Bax-deficient ovaries contained increased numbers of primordial follicles and a trend towards reduced numbers of growing follicles. Bax deficiency led to a reduction in average litter size, and also a reduction in the number of oocytes ovulated in response to exogenous gonadotropins. In contrast, Bax deficiency did not alter follicle atresia. In conclusion, BAX appears to be an important regulator of follicle growth, but is dispensable for follicle atresia in mice.

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The pro-apoptotic gene Bax is required for the death of ectopic primordial germ cells during their migration in the mouse embryo

Cited by 123 publications

References 28 publications

Germ cell specification in mice: signaling, transcription regulation, and epigenetic consequences

Germ cell specification in mice: signaling, transcription regulation, and epigenetic consequences

Foetal germ cells: striking the balance between pluripotency and differentiation

BAX is involved in regulating follicular growth, but is dispensable for follicle atresia in adult mouse ovaries

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