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Allelic reprogramming of chromatin states in human early embryos

National Science Review 2024年第3期11卷 58-71页

作者： Shenli Yuan Lei Gao Wenrong Tao Jianhong Zhan Gang Lu Jingye Zhang Chuanxin Zhang Lizhi Yi Zhenbo Liu Zhenzhen Hou Min Dai Han Zhao Zi-Jiang Chen Jiang Liu Keliang Wu Center for reproductive medicine Shandong University CAS Key laboratory of Genome Sciences and Information Collaborative Innovation Center of Genetics and Development Beijing Institute of Genomicsand China National Center for BioinformationChinese Academy of Sciences University of Chinese Academy of Sciences cuhk-SDU joint laboratory on reproductive Genetics School of Biomedical Sciences the Chinese University of Hong Kong Key laboratory of reproductive Endocrinology of the Ministry of Education Shandong University Center for reproductive medicine Ren Ji Hospital School of Medicine Shanghai Jiao Tong University CAS Center for Excellence in Animal Evolution and Genetics Chinese Academy of Sciences

The reprogramming of parental epigenomes in human early embryos remains elusive. To what extent the characteristics of parental epigenomes are conserved between humans and mice is currently unknown. Here,we mapped parental haploid epigenomes using human parthenogenetic and androgenetic embryos. Human embryos have a larger portion of genome with parentally specific epigenetic states than mouse embryos.The allelic patterns of epigenetic states for orthologous regions are not conserved between humans and mice. Nevertheless, it is conserved that maternal DNA methylation and paternal H3K27me3 are associated with the repression of two alleles in humans and mice. In addition, for DNA-methylation-dependent imprinting, we report 19 novel imprinted genes and their associated germline differentially methylated regions. Unlike in mice, H3K27me3-dependent imprinting is not observed in human early embryos.Collectively, allele-specific epigenomic reprogramming is different in humans and mice.

关键词： human embryo epigenetics reprogramming DNA methylation H3K27me3 chromatin accessibility

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RCAN family member 3 deficiency contributes to noncompaction of the ventricular myocardium

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Journal of Genetics and Genomics 2024年第5期51卷 543-553页

作者： Ting Hu Lan Liu He Wang Mei Yang Bocheng Xu Hanbing Xie Ziyuan Lin Xiaolei Jin Ping Wang Yanyan Liu Huaqin Sun Shanling Liu Department of Medical Genetics West China Second University HospitalSichuan UniversityChengduSichuan 610041China Key laboratory of Birth Defects and Related Diseases of Women and Children(Sichuan University) Ministry of EducationChengduSichuan 610041China Medical College Tibet UniversityLhasaTibet 850000China scu-cuhk joint laboratory for reproductive medicine West China Second University HospitalSichuan UniversityChengduSichuan 610041China West China School of medicine Sichuan UniversityChengduSichuan 610041China

Noncompaction of the ventricular myocardium(NVM),the third most diagnosed cardiomyopathy,is characterized by prominent trabeculae and intratrabecular recesses.However,the genetic etiology of 40%–60%of NVM cases remains unknown.Here,we identify two infants with NVM,in a nonconsanguineous family,with a typical clinical presentation of persistent bradycardia since the prenatal period.A homozygous missense variant(R223L)of RCAN family member 3(RCAN3)is detected in both infants using whole-exome sequencing.In the zebrafish model,marked cardiac dysfunction is detected in rcan3 deficiency(MO-rcan3ATG-injected)and rcan−/−embryos.Developmental dysplasia of both endocardial and myocardial layers is also detected in rcan3-deficient embryos.RCAN3 R223L variant mRNAs can not rescue heart defects caused by rcan3 knockdown or knockout;however,hRCAN3 mRNAs rescue these phenotypes.RNA-seq experiments show that several genes involved in cardiomyopathies are significantly regulated through multiple signaling pathways in the rcan3-knockdown zebrafish model.In human cardiomyocytes,RCAN3 deficiency results in reduced proliferation and increased apoptosis,together with an abnormal mitochondrial ultrastructure.Thus,we suggest that RCAN3 is a susceptibility gene for cardiomyopathies,especially NVM and that the R223L mutation is a potential loss-of-function variant.

关键词： Cardiomyopathy NVM RCAN3 Mitochondrial structure Heartdefects

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Decreased AKAP4/PKA signaling pathway in high DFI sperm affects sperm capacitation

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Asian Journal of Andrology 2024年第1期26卷 25-33页

作者： Kun Zhang Xiu-Hua Xu Jian Wu Ning Wang Gang Li Gui-Min Hao Jin-Feng Cao Hebei Key laboratory of Infertility and Genetics Department of Reproductive MedicineSecond Hospital of Hebei Medical UniversityShijiazhuang 050000China Department of reproductive medicine Affiliated Hospital of Xuzhou Medical UniversityXuzhou 221000China Department of Neurology The 980th Hospital of the People's Liberation Army Joint Logistics Support Force(Bethune International Peace Hospital)Shijiazhuang 050000China.

The sperm DNA fragmentation index(DFI)is a metric used to assess DNA fragmentation within sperm.During in vitro fertilizationembryo transfer(IVF-ET),high sperm DFI can lead to a low fertilization rate,poor embryo development,early miscarriage,etc.A kinase anchoring protein(AKAP)is a scaffold protein that can bind protein kinase A(PKA)to subcellular sites of specific substrates and protects the biophosphorylation reaction.Sperm protein antigen 17(SPA17)can also bind to AKAP.This study intends to explore the reason for the decreased fertilization rate observed in high sperm DFI(H-DFI)patients during IVF-ET.In addition,the study investigates the expression of AKAP,protein kinase A regulatory subunit(PKARIl),and SPA17 between H-DFI and low sperm DFI(L-DFI)patients.SPA17 at the transcriptional level is abnormal,the translational level increases in H-DFI patients,and the expression of AKAP4/PKARIl protein decreases.H,O,has been used to simulate oxidative stress damage to spermatozoa during the formation of sperm DFI.It indicates that H,O,increases the expression of sperm SPA17 protein and suppresses AKAP4/PKARIl protein expression.These processes inhibit sperm capacitation and reduce acrosomal reactions.Embryo culture data and IVF outcomes have been documented.The H-DFI group has a lower fertilization rate.Therefore,the results indicate that the possible causes for the decreased fertilization rate in the H-DFI patients have included loss of sperm AKAP4/PKARIl proteins,blocked sperm capacitation,and reduced occurrence of acrosome reaction.

关键词： AKAP PKA SPA17 sperm capacitation sperm DNA fragmentation index

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LSM14B coordinates protein component expression in the P-body and controls oocyte maturation

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Journal of Genetics and Genomics 2024年第1期51卷 48-60页

作者： Huiru Zhang Tao Zhang Xiang Wan Chang Chen Shu Wang Dongdong Qin Lufan Li Luping Yu Xin Wu State Key laboratory of reproductive medicine and Offspring Health Nanjing Medical UniversityNanjingJiangsu 210029China Center for reproductive medicine and Obstetrics and Gynecology Nanjing Drum Tower HospitalNanjing University Medical SchoolNanjingJiangsu 210029China

The generation of mature and healthy oocytes is the most critical event in the entire female reproductive process,and the mechanisms regulating this process remain to be studied.Here,we demonstrate that Smith-like(LSM)family member 14B(LSM14B)regulates oocyte maturation,and the loss of LSM14B in mouse ovaries leads to abnormal oocyte MII arrest and female infertility.Next,we find the aberrant transcriptional activation,indicated by abnormal non-surrounded nucleolus and surrounded nucleolus oocyte proportions,and abnormal chromosome assembly and segregation in Lsm14b-deficient mouse oocytes.The global transcriptome analysis suggests that many transcripts involved in cytoplasmic processing body(P-body)function are altered in Lsm14b-deficient mouse oocytes.Deletion of Lsm14b results in the expression and/or localization changes of P-body components(such as LSM14A,DCP1A,and 4E-T).Notably,DDX6,a key component of the P-body,is downregulated and accumulates in the nuclei in Lsm14b-deficient mouse oocytes.Taken together,our data suggest that LSM14B links mouse oocyte maturation to female fertility through the regulation of the P-body.

关键词： LSM14B P-body DDX6 MIl arrest Chromatin configuration

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Effect of SARS-CoV-2 infection on semenparameters in sperm bank volunteers with normalsperm concentration

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Asian Journal of Andrology 2024年第3期26卷 328-332页

作者： Li Wang Wen-Kai Han Xiao-Hui Song Qi-Lin Zhang An-Quan Guan Yuan Gao Jin-Long Ma Center for reproductive medicine Shandong UniversityJinan 250001China State Key laboratory of reproductive medicine and Offspring Health ShandongUniversityJinan 250001China Key laboratory of reproductive Endocrinology of Ministry of Education Shandong UniversityJinan 250001China Shandong Keylaboratory of reproductive medicine Shandong Provincial Hospital Affiliated to Shandong First Medical UniversityJinan 250001China Shandong Provincial ClinicalResearch Center for reproductive Health Jinan 250001China Shandong Technology Innovation Center for reproductive Health Jinan 250001China NationalResearch Center for Assisted reproductive Technology and reproductive Genetics Shandong UniversityJinan 250001China Research Unit of Gametogenesis andHealth of ART-Offspring Chinese Academy of Medical Sciences(No.2021RU001)Jinan 250001China.

In this study,we aimed to assess the effect of severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)infection on semenparameters.The study comprised 110 sperm volunteers who self-reported SARS-CoV-2 infection from the Human Sperm Bank ofthe Center for reproductive medicine,Shandong University(Jinan,China).The volunteers had normal sperm concentration beforeinfection.Each volunteer provided semen samples before and after infection.We selected 90 days after infection as the cutoff point.Semen parameters within 90 days after infection of 109 volunteers(group A)were compared with semen parameters before infection.Moreover,semen parameters on or after 90 days after infection of 36 volunteers(group B)were compared with semen parameters beforeinfection.Furthermore,based on whether the volunteers had completed the three-dose SARS-CoV-2 vaccination booster,volunteersin group A and B were further divided into two subgroups separately.Semen parameters were compared before and after infection ineach subgroup.Our results showed that in this cohort population,the semen quality in volunteers with normal sperm concentrationsbefore infection decreased after SARS-CoV-2 infection within 90 days,while the semen quality returned to preinfection levels after 90days.The completion of a three-dose SARS-CoV-2 vaccination booster may exert a protective effect on semen quality after infection.

关键词： SARS-CoV-2 SARS-CoV-2 vaccination semen quality sperm donation sperm parameters

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Cellular atlases of ovarian microenvironment alterations by diet and genetically-induced obesity

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Science China(Life Sciences) 2024年第1期67卷 51-66页

作者： Yonghui Jiang Xueying Gao Yue Liu Xueqi Yan Huangcong Shi Rusong Zhao Zi-Jiang Chen Fei Gao Han Zhao Shigang Zhao Center for reproductive medicine Shandong UniversityJinan 250012China Research Unit of Gametogenesis and Health of ART-Offspring Chinese Academy of Medical Sciences(No.2021RU001)Jinan 250012China Key laboratory of reproductive Endocrinology of Ministry of Education Shandong UniversityJinan 250012China Shandong Key laboratory of reproductive medicine Shandong Provincial Hospital Affiliated to Shandong First Medical UniversityJinan 250012China Shandong Provincial Clinical Research Center for reproductive Health Jinan 250012China National Research Center of Assisted reproductive Technology and reproductive Genetics Shandong UniversityJinan 250012China The Affiliated Suzhou Hospital of Nanjing Medical University Suzhou Municipal HospitalGusu SchoolNanjing Medical UniversitySuzhou 215000China Center for reproductive medicine Ren Ji HospitalSchool of MedicineShanghai Jiao Tong UniversityShanghai 200127China Shanghai Key laboratory for Assisted Reproduction and reproductive Genetics Shanghai 200127China State Key laboratory of Stem Cell and reproductive Biology Institute of ZoologyChinese Academy of ScienceBeijing 100101China

Obesity,which can arise from genetic or environmental factors,has been shown to cause serious damages to the reproductive system.The ovary,as one of the primary regulators of female fertility,is a complex organ comprised of heterogeneous cell types that work together to maintain a normal ovarian microenvironment(OME).Despite its importance,the effect of obesity on the entire ovary remains poorly documented.In this study,we performed ovary single-cell and nanoscale spatial RNA sequencing to investigate how the OME changed under different kinds of obesity,including high-fat diet(HFD)induced obesity and Leptin ablation induced obesity(OB).Our results demonstrate that OB,but not HFD,dramatically altered the proportion of ovarian granulosa cells,theca-interstitial cells,luteal cells,and endothelial cells.Furthermore,based on the spatial dynamics of follicular development,we defined four subpopulations of granulosa cell and found that obesity drastically disrupted the differentiation of mural granulosa cells from small to large antral follicles.Functionally,HFD enhanced follicle-stimulating hormone(FSH)sensitivity and hormone conversion,while OB caused decreased sensitivity,inadequate steroid hormone conversion,and impaired follicular development.These differences can be explained by the differential expression pattern of the transcription factor Foxo1.Overall,our study provides a powerful and high-resolution resource for profiling obesity-induced OME and offers insights into the diverse effects of obesity on female reproductive disorders.

关键词： obesity ovarian microenvironment snRNA-seq Stereo-seq Foxo1

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Identification of two compound heterozygous GNRHR mutations in two siblings with congenital hypogonadotropic hypogonadism

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Asian Journal of Andrology 2024年第1期26卷 120-122页

作者： Xiao-Bin Wang Ping Chen Xue-Er Yu Zu-Liang Yao Ting-Chao Guo Bo-Chen Pan Center for reproductive medicine Department of Obstetrics and GynecologyShengjing Hospital of China Medical UniversityShenyang 110004China NuProbe Shanghai 200433China Urology Surgery of The Affiliated reproductive Hospital of China Medical University and Liaoning Key laboratory of reproductive Health Liaoning Research Institute of Family Planning(The Affiliated Reproductive Hospital of China Medical University)Shenyang 110031China NHC Key laboratory of reproductive Health and Medical Genetics China Medical UniversityShenyang 110122China

DearEditor,Congenital hypogonadotropic hypogonadism(CHH)is a rare genetic disease characterized by gonadotropin-releasing hormone(GnRH)deficiency or insufficiency and normal hypothalamic-pituitary structures,resulting in defective sexual maturation or/and infertility.!CHH presents as a variety of nonreproductive phenotypes,such as renal hypoplasia,dental hypoplasia,or oculomotor abnormalities.

关键词： pogon compound ism

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Pyruvate kinase M in germ cells is essential for sperm motility and male fertility but not spermatogenesis

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Asian Journal of Andrology 2024年第2期26卷 212-219页

作者： Gao-Qing Qian Xiao-Chen Wang Xi Zhang Bin Shen Qiang Liu State Key laboratory of reproductive medicine and Offspring Health Nanjing Medical UniversityNanjing 211166China Shanghai Key laboratory of reproductive medicine Department of HistoembryologyGenetics and Developmental BiologyShanghai Jiao Tong University School of MedicineShanghai 200025China State Key laboratory of Molecular Biology Shanghai Key Laboratory of Molecular AndrologyShanghai Institute of Biochemistry and Cell BiologyCenter for Excellence in Molecular Cell ScienceChinese Academy of SciencesUniversity of Chinese Academy of SciencesShanghai 200031China

Male germ cells employ specific metabolic pathways throughout their developmental stages.In a previous study,we discovered heightened expression of pyruvate kinase M(PKM),a pivotal glycolytic enzyme,in spermatogonia and spermatids.To gain deeper insights into PKM's roles in spermatogenesis,sperm function,and male fertility,we engineered a conditional-knockout mouse model(Pkm-vkO mice)to selectively disrupt the Pkm gene within germ cells.Despite maintaining regular testicular histology and sperm morphology,the male Pkm-vko mice were infertility,characterized by significant impairments in sperm motility and adenosine triphosphate(ATP)generation.In addition,Pkm-null spermatozoa exhibited similar deficits in protein tyrosine phosphorylation linked to capacitation,as well as compromised performance in in vitro fertilization experiments.To conclude,PKM's presence is not obligatory for the entirety of spermatogenesis in male germ cells;however,it emerges as a critical factor influencing sperm motility and overall male fertility.

关键词： glycolysis male fertility pyruvate kinase M sperm motility spermatogenesis

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A Dietary Supplement Jinghuosu Ameliorates reproductive Damage Induced by Tripterygium Glycosides

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Chinese Journal of Integrative medicine 2024年第4期30卷 330-338页

作者： MA Jing SUN Bo TE Li-ger HUANG Xin ZUO Xin HAN Xiao-ke WANG Shu-song Hebei Key laboratory of reproductive medicine Hebei Institute of Reproductive HealthHebei Reproductive Health HospitalShijiazhuang(050071)China Graduate School of Hebei Medical University Shijiazhuang(050017)China School of Chemistry and Materials Science Hebei Normal UniversityShijiazhuang(050024)China Xingtai Infertility Specialist Hospital XingtaiHebei Province(054000)China

Objective To determine the possible protective effects of Jinghuosu,a dietary supplement(DS),on tripterygium glycosides(TG)-induced reproductive system injury in rats and its underlying mechanisms.Methods A reproductive damage model was established in rats by feeding of TGs.Twenty-eight male Sprague Dawley rats were randomly divided into 4 groups using a random number table(n=7 in each):control(C)group,model(M)group,DS group and L-carnitine(LC)group.Rats in M,DS and LC groups received 40 mg/kg TGs orally.Starting from the 5th week,after administration of TGs for 4 h every day,rats in DS and LC groups were administered with 2.7 g/kg DS and 0.21 g/kg LC,respectively,for protective treatment over the next 4 weeks.Rats in Group C continued to receive the control treatment.Hematoxylin-eosin staining was used for histopathological analysis of rat testicular tissues.Enzyme-linked immunosorbent assay was performed to measure alkaline phosphatase(ALP),lactate dehydrogenase,alcohol dehydrogenase,total antioxidant capacity(T-AOC),superoxide dismutase,glutathione peroxidase(GSH-Px),and malondialdehyde(MDA)concentrations.Chemiluminescence assay was used to determine the serum testosterone content.Quantitative real-time PCR and Western blotting were conducted to analyze the expression of genes and proteins related to the testosterone synthesis pathway and the nuclear factor erythroid 2-related factor 2/heme oxygenase 1 antioxidant pathway.Results Oral administration of TGs induced significant increases in the testicular levels of zinc transporter 1 and MDA(P<0.05).On the other hand,sperm concentration,sperm motility,and serum testosterone,serum zinc,testicular zinc,Zrt-,Irt-like protein 1,ALP,luteinizing hormone(LH)receptor,steroidogenic acute regulatory protein,Cytochrome P450 family 11 subfamily A member 1,3β-hydroxysteroid dehydrogenase 1 T-AOC,GSH-Px,nuclear factor erythroid 2-related factor 2,heme oxygenase-1 and NAD(P)H:quinone oxidoreductase 1 levels decreased following TGs exposure(P<0.05).All of these phenotypes were

关键词： dietary supplement Jinghuosu tripterygium glycosides reproductive damage infertility

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Deleterious variants in RNF111 impair female fertility and induce premature ovarian insufficiency in humans and mice

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Science China(Life Sciences) 2024年第7期67卷 1325-1337页

作者： Chengcheng Song Yingying Qin Yan Li Bingyi Yang Ting Guo Wenqing Ma Dian Xu Keyan Xu Fangfang Fu Li Jin Yanhua Wu Shuyan Tang Xiaojun Chen Feng Zhang Obstetrics and Gynecology Hospital State Key Laboratory of Genetic EngineeringInstitute of Medical Genetics and GenomicsFudan UniversityShanghai 200011China Human Phenome Institute Zhangjiang Fudan International Innovation CenterFudan UniversityShanghai 201203China Center for reproductive medicine Cheeloo College of MedicineShandong UniversityJinan 250021China State Key laboratory of reproductive medicine and Offspring Health Key Laboratory of Reproductive Endocrinology of Ministry of EducationNational Research Center for Assisted Reproductive Technology and Reproductive GeneticsShandong Key Laboratory of Reproductive MedicineShandong Provincial Clinical Research Center for Reproductive HealthShandong UniversityJinan 250021China Department of Obstetrics and Gynecology Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China National Demonstration Center for Experimental Biology Education School of Life SciencesFudan UniversityShanghai 200433China Department of Gynecology the Tenth People’s Hospital of Tongji UniversityShanghai 200072China Soong Ching Ling Institute of Maternity and Child Health International Peace Maternity and Child Health Hospital of China Welfare InstituteShanghai 200030China

Premature ovarian insufficiency(POI)is a heterogeneous female disorder characterized by the loss of ovarian function before the age of 40.It represents a significant detriment to female fertility.However,the known POI-causative genes currently account for only a fraction of cases.To elucidate the genetic factors underlying POI,we conducted whole-exome sequencing on a family with three fertile POI patients and identified a deleterious missense variant in RNF111.In a subsequent replication study involving 1,030 POI patients,this variant was not only confirmed but also accompanied by the discovery of three additional predicted deleterious RNF111 variants.These variants collectively account for eight cases,representing 0.78%of the study cohort.A further study involving 500 patients with diminished ovarian reserve also identified two additional RNF111 variants.Notably,RNF111 encodes an E3 ubiquitin ligase with a regulatory role in the TGF-β/BMP signaling pathway.Our analysis revealed that RNF111/RNF111 is predominantly expressed in the oocytes of mice,monkeys,and humans.To further investigate the functional implications of RNF111 variants,we generated two mouse models:one with a heterozygous missense mutation(Rnf111+/M)and another with a heterozygous null mutation(Rnf111^(+/-)).Both mouse models exhibited impaired female fertility,characterized by reduced litter sizes and small ovarian reserve.Additionally,RNA-seq and quantitative proteomics analysis unveiled that Rnf111 haploinsufficiency led to dysregulation in female gonad development and negative regulation of the BMP signaling pathway within mouse ovaries.In conclusion,our findings strongly suggest that monoallelic deleterious variants in RNF111 can impair female fertility and induce POI in both humans and mice.

关键词： POI RNF111 female fertility ovarian reserve

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