TAF4b promotes mouse primordial follicle assembly and oocyte survival

Grive, Kathryn J.; Seymour, Kimberly A.; Mehta, Rajvi; Freiman, Richard N.

doi:10.1016/j.ydbio.2014.05.001

Cited by 37 publications

(37 citation statements)

References 51 publications

(81 reference statements)

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“…Taf4b-deficient female mice are viable but infertile and suffer from many hallmarks of premature ovarian failure, including follicle depletion, persistent estrous and high serum levels of the gonadotropin follicle stimulating hormone (FSH) (Falender et al, 2005;Freiman et al, 2001;Lovasco et al, 2010;Voronina et al, 2007). Recent work has demonstrated that Taf4b-deficient ovaries experience dramatic germ cell loss by apoptosis immediately after birth, the time at which the ovarian reserve is established (Grive et al, 2014). Furthermore, Taf4b-deficient females experience delayed cyst breakdown and defective primordial follicle assembly.…”

Section: The Transcriptional Control Of Primordial Follicle Developmentmentioning

confidence: 99%

“…Impaired cyst breakdown; loss of primordial follicles (Lechowska et al, 2011;Rajkovic et al, 2004;Suzumori et al, 2002) TBP-associated Factor 4b (Taf4b) Impaired cyst breakdown; loss of primordial follicles (Falender et al, 2005;Freiman et al, 2001;Grive et al, 2014;Lovasco et al, 2010;Voronina et al, 2007) …”

Section: Signaling During Primordial Follicle Formationmentioning

confidence: 99%

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The developmental origins of the mammalian ovarian reserve

2015

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The adult mammalian ovary is devoid of definitive germline stem cells. As such, female reproductive senescence largely results from the depletion of a finite ovarian follicle pool that is produced during embryonic development. Remarkably, the crucial nature and regulation of follicle assembly and survival during embryogenesis is just coming into focus. This developmental pathway involves the coordination of meiotic progression and the breakdown of germ cell cysts into individual oocytes housed within primordial follicles. Recent evidence also indicates that genetic and environmental factors can specifically perturb primordial follicle assembly. Here, we review the cellular and molecular mechanisms by which the mammalian ovarian reserve is established, highlighting the presence of a crucial checkpoint that allows survival of only the highest-quality oocytes.

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Section: The Transcriptional Control Of Primordial Follicle Developmentmentioning

confidence: 99%

Section: Signaling During Primordial Follicle Formationmentioning

confidence: 99%

The developmental origins of the mammalian ovarian reserve

2015

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“…Whole ovaries were incubated with TRA98 antibody (BBridge) diluted 1:100 to label germ cells [17,18] and with cleaved PARP (product no. E51; Abcam) diluted 1:100 to label cells undergoing apoptosis overnight and then with goat anti-rat secondary Alexa 488 and goat anti-rabbit Alexa 568, respectively.…”

Section: Tra98 and Cleaved Parp Immunohistochemistrymentioning

confidence: 99%

Lats1 Deletion Causes Increased Germ Cell Apoptosis and Follicular Cysts in Mouse Ovaries1

Sun¹,

Pepling²,

Diaz³

2015

Biology of Reproduction

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The Hippo signaling pathway is essential for regulating proliferation and apoptosis in mammalian cells. The LATS1 kinase is a core member of the Hippo signaling pathway that phosphorylates and inactivates the transcriptional co-activators YAP1 and WWTR1. Deletion of Lats1 results in low neonate survival and ovarian stromal tumors in surviving adults, but the effects of Lats1 on early follicular development are not understood. Here, the expression of Hippo pathway components including Wwtr1, Stk4, Stk3, Lats2, and Yap1 transcripts were decreased by 50% in mouse ovaries between 2 and 8 days of age while expression was maintained from 8 days to 21 days and after priming with eCG. LATS1, LATS2, and MOB1B were localized to both germ and somatic cells of primordial to antral follicles. Interestingly, YAP1 was predominantly cytoplasmic, whereas WWTR1 was nuclear in oocytes and somatic cells. Deletion of Lats1 caused an increase in germ cell apoptosis from 1.7% in control ovaries to 3.6% in Lats1 mutant ovaries and a 58% and 32% decrease in primordial and activated follicle numbers in cultured mutant ovaries. Surprisingly, there was an increase in Bmp15 but not Gdf9, Figla, Nobox transcripts or the somatic-specific transcripts Amh and Wnt4 in cultured Lats1 mutant ovaries. Last, Lats1 mutant ovaries developed ovarian cysts at a higher frequency (43%) than heterozygous (24%) and control ovaries (8%). Results showed that the Hippo pathway is active in ovarian follicles and that LATS1 is required to maintain the pool of germ cells and primordial follicles.

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“…23,25,[28][29][30][31] Several tissue-specific variants of TAFs have been discovered: TAF4 variants are important for ovarian development and spermatogenesis in mice, while Drosophila and human TAF5 and TAF7 paralogs are implicated in male gametogenesis, thus providing the TFIID with unique functions in a tissue-specific transcription environment. [32][33][34][35][36][37] Following the binding of TFIID, TFIIA binds and stabilizes the association of TFIID with the TATA-box. The formation of the TFIID-TFIIA-DNA complex is followed by the sequential binding of TFIIB, RNAP II/TFIIF, TFIIE and TFIIH, resulting in the assembly of the PIC.…”

Section: Introductionmentioning

confidence: 99%

TRF2: TRansForming the view of general transcription factors

et al. 2015

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These authors contributed equally to this work.Keywords: core promoter elements/motifs, DPE, embryonic development, histone gene cluster, RNAP II transcription, ribosomal protein genes, spermiogenesis, TBP-related factors, TRF2, TCT Transcriptional regulation is pivotal for development and differentiation of organisms. Transcription of eukaryotic protein-coding genes by RNA polymerase II (RNAP II) initiates at the core promoter. Core promoters, which encompass the transcription start site, may contain functional core promoter elements, such as the TATA box, initiator, TCT and downstream core promoter element. TRF2 (TATA-box-binding protein-related factor 2) does not bind TATA box-containing promoters. Rather, it is recruited to core promoters via sequences other than the TATA box. We review the recent findings implicating TRF2 as a basal transcription factor in the regulation of diverse biological processes and specialized transcriptional programs.

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TAF4b promotes mouse primordial follicle assembly and oocyte survival

Cited by 37 publications

References 51 publications

The developmental origins of the mammalian ovarian reserve

The developmental origins of the mammalian ovarian reserve

Lats1 Deletion Causes Increased Germ Cell Apoptosis and Follicular Cysts in Mouse Ovaries1

TRF2: TRansForming the view of general transcription factors

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