ArticleCell death & disease2023
PARP1-catalyzed PARylation of YY1 mediates endoplasmic reticulum stress in granulosa cells to determine primordial follicle activation.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Gene regulatory networks orchestrating oocyte fate bifurcation in primordial follicles revealed by single-cell transcriptomics.Communications biology · 2026Article
- Exploration of the dynamic regulation of the hypothalamic-pituitary-ovarian axis during the estrous cycle.Journal of ovarian research · 2026Article
- A Large-Scale Method to Measure the Stoichiometries of Protein Poly-ADP-Ribosylation.ACS chemical biology · 2026Article
- Ferulic Acid Alleviates Chemotherapy-Induced POI by Targeting the Grp78 and Perk-eIF2α-ATF4-CHOP Pathway to Attenuate Endoplasmic Reticulum Stress.Biomedicines · 2026Article
- From Coffee Alkaloid to Ovarian Targets: An Integrated Computational Framework for Trigonelline in Ovarian Aging.Food science & nutrition · 2026Article
- The SP1-SuperEnhancer-SPHK1 Axis Mediates Niraparib Resistance in TNBC.Pharmaceuticals (Basel, Switzerland) · 2025Article
- LncRNA ENST00000532153.1 alleviates podocyte injury by inhibiting PARP1-mediated PARylation of ATF3 in diabetic kidney disease.Cellular and molecular life sciences : CMLS · 2025Article
- PARylation promotes acute kidney injuryActa pharmaceutica Sinica. B · 2025Article
- Targeting programmed cell death with natural products: a potential therapeutic strategy for diminished ovarian reserve and fertility preservation.Frontiers in pharmacology · 2025Review
- Transcription factor YY1 adversely governs ovarian granulosa cell growth in PCOS by transcription activation-mediated CDKN1C upregulation.Functional & integrative genomics · 2024Article
- The adverse role of endocrine disrupting chemicals in the reproductive system.Frontiers in endocrinology · 2023Review
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although only a small number of primordial follicles are known to be selectively activated during female reproductive cycles, the mechanisms that trigger this recruitment remain largely uncharacterized. Misregulated activation of primordial follicles may lead to the exhaustion of the non-renewable pool of primordial follicles, resulting in premature ovarian insufficiency. Here, we found that poly(ADP-ribose) polymerase 1 (PARP1) enzymatic activity in the surrounding granulosa cells (GCs) in follicles determines the subpopulation of the dormant primordial follicles to be awakened. Conversely, specifically inhibiting PARP1 in oocytes in an in vitro mouse follicle reconstitution model does not affect primordial follicle activation. Further analysis revealed that PARP1-catalyzed transcription factor YY1 PARylation at Y185 residue facilitates YY1 occupancy at Grp78 promoter, a key molecular chaperone of endoplasmic reticulum stress (ERS), and promotes Grp78 transcription in GCs, which is required for GCs maintaining proper ERS during primordial follicle activation. Inhibiting PARP1 prevents the loss of primordial follicle pool by attenuating the excessive ERS in GCs under fetal bisphenol A exposure. Together, we demonstrate that PARP1 in GCs acts as a pivotal modulator to determine the fate of the primordial follicles and may represent a novel therapeutic target for the retention of primordial follicle pool in females.
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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.