4.6 Article

CBP-CITED4 is required for luteinizing hormone-triggered target gene expression during ovulation

期刊

MOLECULAR HUMAN REPRODUCTION
卷 20, 期 9, 页码 850-860

出版社

OXFORD UNIV PRESS
DOI: 10.1093/molehr/gau040

关键词

follicle; ovulation; CITED4; MAPK signaling pathway; granulosa cell

资金

  1. National Basic Research Program of China [2011CB944504, 2012CB944403]
  2. National Natural Science Foundation of China [81172473]
  3. Natural Science Foundation of Zhejiang Province [R2100145]
  4. Basic Scientific Research Funding of Zhejiang University [2011QN81001]
  5. NIH [NIH-HD-16229]
  6. NIH as part of the Specialized Cooperative Centers Program in Reproduction and Infertility Research (SCCPIR) [U54-HD-007495]

向作者/读者索取更多资源

Pituitary-secreted luteinizing hormone (LH) induces ovulation by activating an extracellular regulated kinase 1/2 (ERK1/2) cascade. However, little is known regarding the ERK1/2 downstream effectors that are involved in regulating rapid, transient expression of LH-target gene in ovulatory follicles. By comparing the gene expression profiles of LH-stimulated wild type with ERK1/2-deleted ovarian granulosa cells (GCs), we identified Cited4 as a previously unknown LH target gene during ovulation. LH induced Cited4 expression in pre-ovulatory follicles in an ERK1/2-dependent manner. CITED4 formed an endogenous protein complex and docked on the promoters of LH and ERK1/2 target genes. Both CITED4 expression and CBP acetyltransferase activity leading to histone acetylation were indispensable for LH-induced ovulation-related events. LH induced dynamic histone acetylation changes in pre-ovulatory GCs, including the acetylation of histone H2B (Lys5) and H3 (Lys9). This was essential for the rapid responses and dramatic increases of LH target gene expressions by the ordered activation of ERK1/2 and CITED4-CBP. In addition, histonedeacetylases(HDACs) antagonizedCITED4-CBPto turn off expressionof these genes afterexposure to LH. Thus, we determinedthat CITED4 was a novel LH and ERK1/2 target for triggering ovulation. These results support the proposition that LH induces rapid, significant gene expression in pre-ovulatory follicles by modulating histone acetylation status.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.6
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

Article Oncology

Identification of new hypoxia-regulated epithelial-mesenchymal transition marker genes labeled by H3K4 acetylation

Jian-Qiu Wang, Feng-Qin Yan, Li-Hui Wang, Wen-Juan Yin, Ting-Yu Chang, Jun-Ping Liu, Kou-Juey Wu

GENES CHROMOSOMES & CANCER (2020)

Article Biochemistry & Molecular Biology

Chchd2 regulates mitochondrial morphology by modulating the levels of Opa1

Wei Liu, Xiuying Duan, Lingna Xu, Weina Shang, Jiayao Zhao, Liquan Wang, Jian-Chiuan Li, Chun-Hong Chen, Jun-Ping Liu, Chao Tong

CELL DEATH AND DIFFERENTIATION (2020)

Review Pharmacology & Pharmacy

Role of telomerase in the tumour microenvironment

Ning Liu, Xue-Hua Guo, Jun-Ping Liu, Yu-Sheng Cong

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY (2020)

Article Pharmacology & Pharmacy

Molecular insight into the selective binding between human telomere G-quadruplex and a negatively charged stabilizer

Zhiguo Wang, Jianfeng Li, Jun Liu, Lihui Wang, Yanhua Lu, Jun-Ping Liu

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY (2020)

Article Medicine, General & Internal

Epidemiological and clinical features of pediatric COVID-19

Cheng-Xian Guo, Li He, Ji-Ye Yin, Xiang-Guang Meng, Wei Tan, Guo-Ping Yang, Tao Bo, Jun-Ping Liu, Xin-Jian Lin, Xiang Chen

BMC MEDICINE (2020)

Article Biochemistry & Molecular Biology

Pyrroline-5-carboxylate synthase senses cellular stress and modulates metabolism by regulating mitochondrial respiration

Zhaoying Yang, Xiaocui Zhao, Weina Shang, Yang Liu, Jun-Feng Ji, Jun-Ping Liu, Chao Tong

Summary: P5CS, an enzyme responsible for synthesizing pyrroline-5-carboxylate, plays a crucial role in proline and ornithine synthesis. Dysfunctional P5CS can lead to various human diseases, affecting proliferation rate, cellular stress sensitivity, and lipid-droplet accumulation. The study reveals the importance of P5CS in regulating lipid metabolism and mitochondrial respiratory complex organization, shedding light on its role in metabolic disorders.

CELL DEATH AND DIFFERENTIATION (2021)

Article Biochemistry & Molecular Biology

Simultaneous visualisation of the complete sets of telomeres from the MmeI generated terminal restriction fragments in yeasts

Jun Liu, Xiaojing Hong, Chao-Ya Liang, Jun-Ping Liu

Article Biology

Miga-mediated endoplasmic reticulum-mitochondria contact sites regulate neuronal homeostasis

Lingna Xu, Xi Wang, Jia Zhou, Yunyi Qiu, Weina Shang, Jun-Ping Liu, Liquan Wang, Chao Tong

Article Cell Biology

Sir4 Deficiency Reverses Cell Senescence by Sub-Telomere Recombination

Jun Liu, Xiaojing Hong, Lihui Wang, Chao-Ya Liang, Jun-Ping Liu

Summary: Telomere shortening leads to cellular senescence, and this study reveals a dual opposing control mechanism of sub-telomeric Y' element recombination by Sir3/4 and Rif1, regulating telomere length and cell senescence in yeast Saccharomyces cerevisiae. Sir4 repression of Y' element recombination is negatively regulated by Rif1, mediating senescence-evasion induced by Sir4 deficiency.
Review Pharmacology & Pharmacy

Mechanisms of cancer stem cell senescence: Current understanding and future perspectives

Da-Yong Zhang, Michael J. Monteiro, Jun-Ping Liu, Wen-Yi Gu

Summary: CSCs, a small population of tumor cells with self-renewal and aberrant differentiation abilities, play crucial roles in tumor development and recurrence. Research indicates that CSCs can undergo cell senescence, allowing them to evade the cytotoxic effects of cancer therapy.

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY (2021)

Article Cell Biology

Regulation of lipid homeostasis by the TBC protein dTBC1D22 via modulation of the small GTPase Rab40 to facilitate lipophagy

Xiuying Duan, Lingna Xu, Yawen Li, Lijun Jia, Wei Liu, Wenxia Shao, Vafa Bayat, Weina Shang, Liquan Wang, Jun-Ping Liu, Chao Tong

Summary: Through experiments involving overexpression and mutations, it was found that dTBC1D22 interacts with Rab40, regulating lipid droplet accumulation and mobilization, dependent on the distribution of Lamp1. The impact of Rab40 on lipophagy and Golgi function may lead to lipid homeostasis imbalance.

CELL REPORTS (2021)

Article Cell Biology

Pulmonary Alveolar Stem Cell Senescence, Apoptosis, and Differentiation by p53-Dependent and -Independent Mechanisms in Telomerase-Deficient Mice

Kexiong Zhang, Lihui Wang, Xiaojing Hong, Hao Chen, Yao Shi, Yingying Liu, Jun Liu, Jun-Ping Liu

Summary: The Telomerase RNA component (TERC) knockout leads to p53-dependent premature replicative senescence and apoptosis of pulmonary stem cells, which can be significantly reduced by p53 deficiency. These findings demonstrate the association between TERC deficiency-induced telomere DDR and pulmonary aging.
Review Cell Biology

Molecular Mechanisms of Alveolar Epithelial Stem Cell Senescence and Senescence-Associated Differentiation Disorders in Pulmonary Fibrosis

Xiaojing Hong, Lihui Wang, Kexiong Zhang, Jun Liu, Jun-Ping Liu

Summary: Pulmonary senescence, accelerated by unresolved DNA damage response, increases susceptibility to pulmonary fibrosis. Recent studies have shown that SARS-Cov-2 viral infection induces acute pulmonary epithelial senescence followed by fibrosis, although the underlying mechanism is unclear. This study explores the roles of alveolar epithelial stem cell senescence and senescence-associated differentiation disorders in pulmonary fibrosis, and investigates the mechanisms involved in mediating and preventing fibrogenic crisis. The TGF-beta signaling pathway mediates alveolar epithelial stem cell senescence through suppression of the telomerase reverse transcriptase gene, while telomere uncapping caused by stress-induced telomeric shelterin protein TPP1 degradation mediates DNA damage response, pulmonary senescence, and fibrosis. Targeted intervention of cellular senescence disrupts pulmonary remodeling and fibrosis by clearing senescent cells or preventing senescence using telomere dysfunction inhibitor (TELODIN). Studies suggest that senescence-associated differentiation disorders can be reprogrammed and reversed by inhibiting stem cell replicative senescence in pulmonary fibrosis, providing a framework for targeted intervention of the molecular mechanisms of alveolar stem cell senescence and pulmonary fibrosis.
Article Biochemical Research Methods

Identification of peptidomimetic telomere dysfunction inhibitor (TELODIN) through telomere dysfunction- induced foci (TIF) assay

Lihui Wang, Zhiguo Wang, Jun -Ping Liu

Summary: The study utilized the TIF assay to screen synthetic peptides to prevent telomere dysfunctions caused by environmental radiation, demonstrating a potential intervening therapeutic drug candidate. This work presents a novel approach for identifying telomere dysfunction inhibitors.

STAR PROTOCOLS (2021)

暂无数据