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Differential regulation of H3S10 phosphorylation, mitosis progression and cell fate by Aurora Kinase B and C in mouse preimplantation embryos

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Protein & cell 2017年第9期8卷 662-674页

作者： Wenzhi Li Peizhe Wang Bingjie Zhang Jing Zhang Jia Ming Wei Xie Jie Na Center for Stem cell Biology and Regenerative Medicine School of Medicine Tsinghua University Beijing 100084 China Center for Stem cell Biology and Regenerative Medicine MOE Key Laboratory of Bioinformatics THU-PKU Center for LifeSciences School of Life Sciences Tsinghua University Beijing 100084 China

Coordination of cell division and cell fate is crucial for the successful development of mammalian early embryos. Aurora kinases are evolutionarily conserved serine/threonine kinases and key regulators of mitosis. Aurora kinase B （AurkB） is ubiquitously expressed while Aurora kinase C （AurkC） is specifically expressed in gametes and preimplantation embryos. We found that increasing AurkC level in one blastomere of the 2-cell embryo accelerated cell division and decreasing AurkC level slowed down mitosis. Changing AurkB level had the opposite effect. The kinase domains of AurkB and AurkC were responsible for their different ability to phosphorylate Histone H3 Serine 10 （H3S10P） and regulate metaphase timing. Using an Oct4-photoactivat- able GFP fusion protein （Oct4-paGFP） and fluorescence decay after photoactivation assay, we found that AurkB overexpression reduced Oct4 retention in the nucleus. Finally, we show that blastomeres with higher AurkC level elevated pluripotency gene expression, which were inclined to enter the inner cell mass lineage and subsequently contributed to the embryo proper. Collectively, our results are the first demonstration that the activity of mitotic kinases can influence cell fate decisions in mammalian preimplantation embryos and have important implications to assisted reproduction.

关键词： Aurora kinase mouse preimplantation embryo cell fate development mitosis

Putting things in place for fertilization： discovering roles for importin proteins in cell fate and spermatogenesis

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Asian Journal of Andrology 2015年第4期17卷 537-544页

作者： Kate L Loveland Andrew T Major Romaly Butler Julia C Young David A Jan Yoichi Miyamoto Department of Biochemistry and Molecular Biology Monash University Clayton VIC Australia Department of Anatomy and Developmental Biology Monash UniversityClayton VlC Australia Hudson Institute of Medical Research Monash Medical Centre Clayton VlC Australia School of Clinical Sciences Monash University ClaytonVlC Laboratory of Nuclear Transport Dynamics National Institutes of Biomedical Innovation Health and Nutrition Osaka Japan.

Importin proteins were originally characterized for their central role in protein transport through the nuclear pores, the only intracellular entry to the nucleus. This vital function must be tightly regulated to control access by transcription factors and other nuclear proteins to genomic DNA, to achieve appropriate modulation of cellular behaviors affecting cell fate. Importin-mediated nucleocytoplasmic transport relies on their specific recognition of cargoes, with each importin binding to distinct and overlapping protein subsets. Knowledge of importin function has expanded substantially in regard to three key developmental systems： embryonic stem cells, muscle cells and the germ line. In the decade since the potential for regulated nucleocytoplasmic transport to contribute to spermatogenesis was proposed, we and others have shown that the importins that ferry transcription factors into the nucleus perform additional roles, which control cell fate. This review presents key findings from studies of mammalian spermatogenesis that reveal potential new pathways by which male fertility and infertility arise. These studies of germline genesis illuminate new ways in which importin proteins govern cellular differentiation, includ ng v a d rect ng proteins to d st nct ntrace ular compartments and by determining cellular stress responses.

关键词： cell fate cell stress importin karyopherin nucleocytoplasmic transport spermatid spermatocyte spermatogenesis

pRb-E2F signaling in life of mesenchymal stem cells:cell cycle,cell fate,and cell differentiation

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Genes & Diseases 2014年第2期1卷 174-187页

作者： Boris Popov Nikolay Petrov Institute of Cytology Russian Academy of SciencesSt.Petersburg4Tikhoretsky Av.194064Russia

Mesenchymal stem cells(MSCs)are multipotent cells that can differentiate into various mesodermal lines forming fat,muscle,bone,and other lineages of connective tissue.MSCs possess plasticity and under special metabolic conditions may transform into cells of unusual phenotypes originating from ecto-and endoderm.After transplantation,MSCs release the humoral factors promoting regeneration of the damaged tissue.During last five years,the numbers of registered clinical trials of MSCs have increased about 10 folds.This gives evidence that MSCs present a new promising resource for cell therapy of the most dangerous diseases.The efficacy of the MSCs therapy is limited by low possibilities to regulate their conversion into cells of damaged tissues that is implemented by the pRb-E2F signaling.The widely accepted viewpoint addresses pRb as ubiquitous regulator of cell cycle and tumor suppressor.However,current publications suggest that basic function of the pRb-E2F signaling in development is to regulate cell fate and differentiation.Through facultative and constitutive chromatin modifications,pRb-E2F signaling promotes transient and stable cells quiescence,cell fate choice to differentiate,to senesce,or to die.Loss of pRb is associated with cancer cell fate.pRb regulates cell fate by retaining quiescence of one cell population in favor of commitment of another or by suppression of genes of different cell phenotype.pRb is the founder member of the“pocket protein”family possessing functional redundancy.Critical increase in the efficacy of the MSCs based cell therapy will depend on precise understanding of various aspects of the pRb-E2F signaling.

关键词： cell cycle cell differentiation cell fate Mesenchymal stem cells pRb-E2F signaling

The second polar body contributes to the fate asymmetry in the mouse embryo

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National Science Review 2022年第7期9卷 32-42页

作者： Hongbin Jin Yang Han Huasong Wang J.Xiao He Li Weimin Shen Lin Zhang Luxi Chen Shunji Jia Ping Yuan Hui Chen Anming Meng Laboratory of Molecular Developmental Biology State Key Laboratory of Membrane BiologyTsinghua-Peking Center for Life Sciences School of Life SciencesTsinghua University Center for Reproductive Genetics and Reproductive Medicine Sun Yat-sen Memorial HospitalSun Yat-sen University Guangzhou Laboratory

The polar bodies(PBs) are extruded microcells during oocyte meiosis and generally regarded as inessentials for embryonic development.Therefore,PBs have been widelyused as important materials for pre-implantation genetic diagnosis in human.Here we report that the second PB(PB2) in the mouse zygote may play roles in cell-fate specification and post-implantation development.A subset of mRNAs encoding pluripotency-related factors are enriched in PB2.Nascent proteins maybe synthesized in PB2 after fertilization and transport from PB2 to the zygote before the two-cell stage.The PB2-attached blastomere(pbB) at the two-cell stage,compared to the other blastomere(npbB),likely contributes more descendants to the inner cell mass(ICM) lineage in the blastocyst.Removal of PB2 from the zygote or transient blockage of material exchange between PB2 and the zygote by nocodazole treatment appears to cause a loss of the ICM fate bias of pbB.PB2 removal or nocodazole treatment also results in abnormal post-implantation development.Injection of PB2 lysate into pbB of PB2-removed two-cell-stage embryos may reset the cell-fate preference and rescue post-implantation development.Our data collectively suggest that PB2 would demarcate the earliest cell-fate asymmetry of the mouse zygote and be required for post-implantation development.

关键词： mouse embryo polar body cell fate asymmetry

The cold-induced factor CBF3 mediates root stem cell activity,regeneration,and developmental responses to cold

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Plant Communications 2023年第6期4卷 197-211页

作者： Pablo Perez-Garcia Ornella Pucciariello Alvaro Sanchez-Corrionero Javier Cabrera Cristina del Barrio Juan Carlos del Pozo Mariano Perales Krzysztof Wabnik Miguel A.Moreno-Risueno Centro de Biotecnologíay Genómica de Plantas(Universidad Politécnica de Madrid(UPM)–Instituto Nacional de Investigacióny Tecnología Agraria y Alimentaria–CSIC(INIA-CSIC)) MadridSpain

Plant growth and development involve the specification and regeneration of stem cell niches(SCNs).Although plants are exposed to disparate environmental conditions,how environmental cues affect developmental programs and stem cells is not well understood.Root stem cells are accommodated in meristems in SCNs around the quiescent center(QC),which maintains their activity.Using a combination of genetics and confocal microscopy to trace morphological defects and correlate them with changes in gene expression and protein levels,we show that the cold-induced transcription factor(TF)C-REPEAT BINDING FACTOR 3(CBF3),which has previously been associated with cold acclimation,regulates root development,stem cell activity,and regeneration.CBF3 is integrated into the SHORT-ROOT(SHR)regulatory network,forming a feedback loop that maintains SHR expression.CBF3 is primarily expressed in the root endodermis,whereas the CBF3 protein is localized to other meristematic tissues,including root SCNs.Complementation of cbf3-1 using a wild-type CBF3 gene and a CBF3 fusion with reduced mobility show that CBF3 movement capacity is required for SCN patterning and regulates root growth.Notably,cold induces CBF3,affecting QC activity.Furthermore,exposure to moderate cold around 10℃–12℃promotes root regeneration and QC respecification in a CBF3-dependent manner during the recuperation period.By contrast,CBF3 does not appear to regulate stem cell survival,which has been associated with recuperation from more acute cold(-4℃).We propose a role for CBF3 in mediating the molecular interrelationships among the cold response,stem cell activity,and development.

关键词： stem cells regeneration organ patterning protein movement cell fate low temperature

A self-activation loop maintains stem cell fate for branching

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A self-activation loop maintains stem cell fate for branchin...

Steering Against Wind： A New Network of NamiRNAs and Enhancers

2018全国植物生物学大会

作者： Xiuwei Cao Yuling Jiao State Key Laboratory of Plant Genomics Institute of Genetics and Developmental BiologyChinese Academy of Sciences

Plants differ from most animals in their retained ability to initiate new cycles of growth and development,which relies on the establishment and activity of branch meristems.In seed plants,branching is achieved by axillary meristems,which are established in the axil of each leaf base and develop into lateral branches.Axillary meristems are initiated from a meristematic cell population originally detached from the shoot apical meristem.It remains unclear how the meristematic cell fate is maintained.Here we show that the meristem marker gene SHOOT MERISTEMLESS(STM) can activates its own expression to enable cell fate maintenance.Furthermore,the self-activation loop requires an STM-interacting protein FEWER AXILLARY BRANCHING(FAB),whose mutants display compromised axillary bud formation.Genetic and biochemical data suggest that the STM-FAB heterodimer binds and activates STM as well as additional axillary meristem regulatory genes.Taken together,our finding provides a striking example in which a self-activation loop maintains the meristematic cell fate to enable branching.

关键词： meristem stem cell cell lineage cell fate branching

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Genomics, Proteomics & Bioinformatics 2017年第5期15卷 331-337页

作者： ying liang qingping zou wenqiang yu Laboratory of RNA Epigenetics.Institutes of Biomedical Sciences&Department of General Surgery Huashan Hospital Cancer M etastasis Institute Fudan UniversityShanghai 200032China Department of Biochemistry and Molecular Biology Shanghai Medical College MOE Key Laboratory of Metabolism and Molecular MedicineDepartment of Molecular BiologyFudan UniversityShanghai 200032China Collaborative Innovation Center for Genetics and Development School of Life SciencesFudan UniversityShanghai 200433China

MicroRNAs （miRNAs） are a class of endogenous non-coding RNAs with regulatory functions. Traditionally, miRNAs are thought to play a negative regulatory role in the cytoplasm by binding to the YUTR of target genes to degrade mRNA or inhibit translation. However, it remains a challenge to interpret the potential function of many miRNAs located in the nucleus. Recently, we reported a new type of miRNAs present in the nucleus, which can activate gene expres- sion by binding to the enhancer, and named them nuclear activating miRNAs （NamiRNAs）. The discovery of NamiRNAs showcases a complementary regulatory mechanism of miRNA, demon- strating their differential roles in the nucleus and cytoplasm. Here, we reviewed miRNAs in nucleus to better understand the function of NamiRNAs in their interactions with the enhancers. Accord- ingly, we propose a NamiRNA--enhancer-target gene activation network model to better under- stand the crosstalk between NamiRNAs and enhancers in regulating gene transcription. Moreover, we hypothesize that NamiRNAs may be involved in cell identity or cell fate determina- tion during development, although further study is needed to elucidate the underlying mechanisms in detail.

关键词： Nuclear activating miRNAs Tissue-specific enhancers Transcriptional gene activa-tion cell identity cell fate

Polydendrocytes in development and myelin repair

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Neuroscience Bulletin 2013年第2期29卷 165-176页

作者： Hao Zuo Akiko Nishiyama Department of Physiology and Neurobiology University of Connecticut University of Connecticut Stem cell Institute

Polydendrocytes （NG2 cells） are a distinct type of glia that populate the developing and adult central nervous systems （CNS）. In the adult CNS, they retain mitotic activity and represent the largest proliferating cell popula- tion. Genetic and epigenetic mechanisms regulate the fate of polydendrocytes, which give rise to both oligo- dendrocytes and astrocytes. In addition, polydendrocytes actively differentiate into myelin-forming oligodendro- cytes in response to demyelination. This review summarizes the current knowledge regarding polydendrocyte development, which provides an important basis for understanding the mechanisms that lead to the remyelina- tion of demyelinated lesions.

关键词： polydendrocytes NG2 cells oligodendrocytes myelin cell fate

Progenies of NG2 glia: what do we learn from transgenic mouse models ?

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Neural Regeneration Research 2021年第1期16卷 43-48页

作者： Qilin Guo Anja Scheller Wenhui Huang Molecular Physiology Center for Integrative Physiology and Molecular Medicine(CIPMM)University of SaarlandHomburgGermany

In the mammalian central nervous system,nerve-glia antigen 2(NG2)glia are considered the fourth glial population in addition to astrocytes,oligodendrocytes and microglia.The fate of NG2 glia in vivo has been carefully studied in several transgenic mouse models using the Cre/loxP strategy.There is a clear agreement that NG2 glia mainly serve as progenitors for oligodendrocytes and a subpopulation of astrocytes mainly in the ventral forebrain,whereas the existence of a neurogenic potential of NG2 glia is lack of adequate evidence.This mini review summarizes the findings from recent studies regarding the fate of NG2 glia during development.We will highlight the age-and-region-dependent heterogeneity of the NG2 glia differentiation potential.We will also discuss putative reasons for inconsistent findings in various transgenic mouse lines of previous studies.

关键词： astrogliogenesis cell fate Cre/loxP system development differentiation embryonic brain neurogenesis NG2 glia oligodendrocyte lineage oligodendrocyte precursor cells