ArticleDevelopment (Cambridge, England)2016
JNK signaling regulates E-cadherin junctions in germline cysts and determines primordial follicle formation in mice.
Article in Development (Cambridge, England), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
29 citing papers in PubMed, 43 citations in OpenAlex.
- Attack of the kinases: JNK signaling in metabolism.American journal of physiology. Regulatory, integrative and comparative physiology · 2026Review
- Building a resilient ovarian reserve: Early soma-oocyte interactions.Current topics in developmental biology · 2026Review
- Evaluating Selective Quality Control in Mammalian Oogenesis: Evidence and Opportunities.Annual review of genetics · 2025Review
- CCAAT/enhancer binding protein beta (C/EBPβ) regulates the formation of the ovarian reserve.Communications biology · 2025Article
- The roles of MAPK signaling pathway in ovarian folliculogenesis.Journal of ovarian research · 2025Review
- Chromatin remodeler CHD4 establishes chromatin states required for ovarian reserve formation, maintenance and male germ cell survival.Nucleic acids research · 2025Article
- HFM1 is essential for the germ cell intercellular bridge transport in primordial follicle formation in mice.Cellular and molecular life sciences : CMLS · 2024Article
- Premeiotic deletion of Eif2s2 causes oocyte arrest at the early diplotene stage and apoptosis in mice.Cell proliferation · 2024Article
- Single-cell sequencing reveals the transcriptional alternations of 17β-estradiol suppressing primordial follicle formation in neonatal mouse ovaries.Cell proliferation · 2024Article
- Chromatin remodeler CHD4 establishes chromatin states required for ovarian reserve formation, maintenance, and germ cell survival.bioRxiv : the preprint server for biology · 2024Article
- Identification and analysis of key circRNAs in the mouse embryonic ovary provides insight into primordial follicle development.BMC genomics · 2024Article
- Differentially expressed transcripts study during pregnancy and postpartum anestrus of yak (Animal biotechnology · 2023Article
- Single-cell RNA-seq identified novel genes involved in primordial follicle formation.Frontiers in endocrinology · 2023Article
- Regulation of mouse primordial follicle formation by signaling through the PI3K pathway†.Biology of reproduction · 2022Article
- HB-EGF induces mitochondrial dysfunction via estrogen hypersecretion in granulosa cells dependent on cAMP-PKA-JNK/ERK-CaInternational journal of biological sciences · 2022Article
- Regulation of primordial follicle formation, dormancy, and activation in mice.The Journal of reproduction and development · 2021Review
- Primordial Follicle Formation - Some Assembly Required.Current opinion in endocrine and metabolic research · 2021Article
- Pathophysiological Significance of WDR62 and JNK Signaling in Human Diseases.Frontiers in cell and developmental biology · 2021Review
- Article
- The Central Role of Cadherins in Gonad Development, Reproduction, and Fertility.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Physiologically, the size of the primordial follicle pool determines the reproductive lifespan of female mammals, while its establishment largely depends on a process of germline cyst breakdown during the perinatal period. The mechanisms regulating this process are poorly understood. Here we demonstrate that c-Jun amino-terminal kinase (JNK) signaling is crucial for germline cyst breakdown and primordial follicle formation. JNK was specifically localized in oocytes and its activity increased as germline cyst breakdown progressed. Importantly, disruption of JNK signaling with a specific inhibitor (SP600125) or knockdown technology (Lenti-JNK-shRNAs) resulted in significantly suppressed cyst breakdown and primordial follicle formation in cultured mouse ovaries. Our results show that E-cadherin is intensely expressed in germline cysts, and that its decline is necessary for oocyte release from the cyst. However, inhibition of JNK signaling leads to aberrantly enhanced localization of E-cadherin at oocyte-oocyte contact sites. WNT4 expression is upregulated after SP600125 treatment. Additionally, similar to the effect of SP600125 treatment, WNT4 overexpression delays cyst breakdown and is accompanied by abnormal E-cadherin expression patterns. In conclusion, our results suggest that JNK signaling, which is inversely correlated with WNT4, plays an important role in perinatal germline cyst breakdown and primordial follicle formation by regulating E-cadherin junctions between oocytes in mouse ovaries.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.