Journal of Cell Science Impact Factor & Information

Publisher: Company of Biologists, Company of Biologists

Journal description

Journal of Cell Science covers the complete range of topics in cell biology and is also of key interest to developmental biologists, molecular biologists and geneticists. It is one of the leading journals in the field, and its impact factor is rising steadily. Each issue includes research articles, as well as review articles commissioned from experts in particular fields, brief syntheses of important areas and topical comment. Journal of Cell Science is published twice monthly (24 issues/year).

Current impact factor: 5.43

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 5.432
2013 Impact Factor 5.325
2012 Impact Factor 5.877
2011 Impact Factor 6.111
2010 Impact Factor 6.29
2009 Impact Factor 6.144
2008 Impact Factor 6.247
2006 Impact Factor 6.427
2005 Impact Factor 6.543
2004 Impact Factor 6.91
2003 Impact Factor 7.25
2002 Impact Factor 6.954
2001 Impact Factor 6.213
2000 Impact Factor 5.996
1999 Impact Factor 6.044
1998 Impact Factor 5.453
1997 Impact Factor 5.081
1996 Impact Factor 4.935
1995 Impact Factor 4.827
1994 Impact Factor 4.336
1993 Impact Factor 3.432
1992 Impact Factor 3.593

Impact factor over time

Impact factor

Additional details

5-year impact 6.00
Cited half-life 8.80
Immediacy index 0.93
Eigenfactor 0.09
Article influence 2.53
Website Journal of Cell Science website
Other titles Journal of cell science (Online), Journal of cell science
ISSN 1477-9137
OCLC 37637228
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Company of Biologists

  • Pre-print
    • Author cannot archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • On author's personal website immediately
    • If mandated by a funding agency or institution, the author's post-print may be deposited in designated repository after a 12 months embargo period or as mandated
    • Authors retain copyright
    • Publisher's version/PDF cannot be used
    • Must link to publisher version
    • Publisher will deposit the final publisher version in PMC for authors funded by RCUK, HHMI, NIH, MRC, Wellcome Trust for release 6 or 12 months after publication (as mandated) or immediately upon payment of fee.
    • Non-commercial use
  • Classification
    ​ blue

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Cell surface area rapidly increases during mechanical and hypoosmotic stresses. Such expansion of the plasma membrane requires 'membrane reservoirs' that provide surface area and buffer membrane tension, but the sources of this membrane remain poorly understood. In principle, the flattening of invaginations and buds within the plasma membrane could provide this additional surface area, as recently shown for caveolae in animal cells. Here, we used microfluidics to study rapid expansion of the yeast plasma membrane in protoplasts, which lack the rigid cell wall. To survive hypoosmotic stress, yeast cell protoplasts required eisosomes, protein-based structures that generate long invaginations at the plasma membrane. Both budding yeast and fission yeast protoplasts lacking eisosomes were unable to expand like wild type protoplasts during hypoosmotic stress, and subsequently lysed. By quantitative fluorescence microscopy on single protoplasts, we observed disassembly of eisosomes as surface area increased. During this process, invaginations generated by eisosomes at the plasma membrane became flattened, as visualized by scanning electron microscopy. We propose that eisosomes serve as tension-dependent membrane reservoirs for expansion of yeast cells, analogous to caveolae in animal cells.
    Journal of Cell Science 09/2015; DOI:10.1242/jcs.176867
  • [Show abstract] [Hide abstract]
    ABSTRACT: β-catenin transduces the Wnt signaling pathway and its nuclear accumulation leads to gene transactivation and cancer. Rac1 GTPase is known to stimulate β-catenin dependent transcription of Wnt target genes and we confirmed this activity. Here we tested the recent hypothesis that Rac1 augments Wnt signaling by enhancing β-catenin nuclear import, however we found that silencing/inhibition or up-regulation of Rac1 had no influence on nuclear accumulation of β-catenin. To better define the role of Rac1, we employed proximity ligation assays (PLA) and discovered that a significant pool of Rac1-β-catenin protein complexes redistribute from the plasma membrane to the nucleus upon Wnt or Rac1 activation. More importantly, active Rac1 was shown to stimulate the formation of nuclear β-catenin-LEF-1 complexes. This regulation required Rac1-dependent phosphorylation of β-catenin at specific serines, which when mutated (S191A and S605A) reduced β-catenin binding to LEF-1 by up to 50%, as revealed by PLA and immunoprecipitation experiments. We propose that Rac1-mediated phosphorylation of β-catenin stimulates Wnt dependent gene transactivation by enhancing β-catenin-LEF-1 complex assembly, providing new insight into the mechanism of cross-talk between Rac1 and canonical Wnt/β-catenin signaling.
    Journal of Cell Science 09/2015; DOI:10.1242/jcs.167742
  • [Show abstract] [Hide abstract]
    ABSTRACT: The MEF2-HDAC axis is a master regulator of different developmental programs and adaptive responses in adults. In this manuscript we have investigated the contribution of the axis to the regulation of epithelial morphogenesis, using 3D organotypic cultures of MCF10A cells as a model. We have demonstrated that MEF2 transcriptional activity is up-regulated during acini formation, concomitantly to the exit from the proliferative phase. Up-regulation of MEF2-trascription is coupled to a down-regulation of HDAC7, which occurs independently from changes in mRNA levels, proteasome or autophagy mediated degradation. During acini formation the MEF2-HDAC axis contributes to promote cell cycle exit, through the engagement of the CDK inhibitor CDKN1A. Only in proliferating cells HDAC7 can bind the first intron of the CDKN1A gene, a region characterized by epigenetic markers of active promoters/enhancers. In cells transformed by the oncogene HER2 acini morphogenesis is altered, MEF2 transcription is repressed and HDAC7 is continuously expressed. Importantly reactivation of MEF2 transcriptional activity in these cells, through the use of a HER2 inhibitor or by enhancing MEF2 function reverted the proliferative defect and re-established a normal acini morphogenesis.
    Journal of Cell Science 09/2015; DOI:10.1242/jcs.170357
  • [Show abstract] [Hide abstract]
    ABSTRACT: Seedlings of large-seeded plants are considered to withstand abiotic stresses efficiently. The molecular mechanisms that underlie the involved signaling cross-talk between the large-seeded trait and abiotic tolerance are, however, largely unknown. Here, we demonstrate the molecular link that integrates plant ABA responses to drought stress into a regulation of seed mass. Both loss-of function mutants of ARF2 (Auxin Response Factor 2) transcription repressor and ANT (AINTEGUMENTA transcription factor) over-expression lines exhibited large seed and drought tolerant phenotypes as a result of abnormal ABA-auxin cross-talk signaling pathways in Arabidopsis. The target gene COR15a (COLD-REGULATED15A) was identified to participate the regulation of seed development with ABA signaling through a negative regulation mediated by ANT. Molecular and genetic evidence was presented that suggested ARF2, ANT, and COR15A form an ABA-mediated signaling pathway for the link between the seed mass modulation and drought tolerance. These observations indicate that the ARF2 transcription factor serves as a molecular link that integrates plant ABA responses to drought stress into regulation of seed mass.
    Journal of Cell Science 09/2015; DOI:10.1242/jcs.171207
  • [Show abstract] [Hide abstract]
    ABSTRACT: The S. cerevisiae kinesin Kip2 stabilises astral microtubules and facilitates spindle positioning through transport of microtubule-associated proteins, such as the yeast CLIP-170 homologue Bik1, dynein and the Adenomatous Polyposis Coli-related protein Kar9 to the plus ends of astral microtubules.Here, we show that Kip2 associates physically with its processivity factor Bim1, the yeast homologue of the EB1 plus end-tracking protein. This interaction requires an EB1-binding motif in the N-terminal extension of Kip2 and is negatively regulated by phosphorylation through Mck1, the yeast Glycogen Synthase Kinase 3. In addition, Mck1-dependent phosphorylation decreases the intrinsic microtubule affinity of Kip2. Reduction in Kip2 phosphorylation leads to stabilisation of astral microtubules and accumulation of Kip2, dynein and Kar9 at microtubule plus ends, while loss of Mck1 function leads to defects in spindle positioning. Furthermore, we provide evidence that a subpopulation of Mck1 at the bud-cortex phosphorylates Kip2. We propose that yeast GSK-3 spatially controls astral microtubule dynamics and the loading of dynein and Kar9 on astral microtubule plus ends by regulating Kip2 interactions with Bim1 and microtubules.
    Journal of Cell Science 09/2015; DOI:10.1242/jcs.166686
  • [Show abstract] [Hide abstract]
    ABSTRACT: Eukaryotic initiation factor 6 (eIF6) is a pivotal regulator of ribosomal function, participating in translational control. Previously our data suggest that eIF6 acts as a key binding protein of P311 (a hypertrophic scar-related protein). However, a comprehensive investigation of its functional role and the underlying mechanisms in modulation myofibroblast (a key effector of hypertrophic scar formation) differentiation remains unclear. Here, we identified that eIF6 is a novel regulator of the TGF-β1 expression at transcription level, which has a key role in myofibroblast differentiation. Mechanistically, this effect is associated with eIF6 altering the occupancy of the TGF-β1 promoter by H2A.Z and Sp1. Accordingly, modulation of eIF6 expression in myofibroblasts significantly affects their differentiation via the TGF-β/Smad signaling pathway, which was verified in vivo by the observation that heterozygote eIF6(+/-) mice exhibited enhanced TGF-β1 production coupled with increased α-SMA(+) myofibroblasts after skin injury. Overall, our data reveal that a novel transcriptional regulatory mechanism of eIF6 that acts on facilitating Sp1 recruitment to TGF-β1 promoter via H2A.Z depletion and thus results in increased TGF-β1 transcription, which contributes to myofibroblast differentiation.
    Journal of Cell Science 09/2015; DOI:10.1242/jcs.174870
  • [Show abstract] [Hide abstract]
    ABSTRACT: Collagen VI represents a remarkable extracellular matrix molecule, and in the past few years, studies of this molecule have revealed its involvement in a wide range of tissues and pathological conditions. In addition to its complex multi-step pathway of biosynthesis and assembly that leads to the formation of a characteristic and distinctive network of beaded microfilaments in the extracellular matrix, collagen VI exerts several key roles in different tissues. These range from unique biomechanical roles to cytoprotective functions in different cells, including myofibers, chondrocytes, neurons, fibroblasts and cardiomyocytes. Indeed, collagen VI has been shown to exert a surprisingly broad range of cytoprotective effects, which include counteracting apoptosis and oxidative damage, favoring tumor growth and progression, regulating autophagy and cell differentiation, and even contributing to the maintenance of stemness. In this Cell Science at a Glance article and the accompanying poster, we present the current knowledge of collagen VI, and in particular, discuss its relevance in stemness and in preserving the mechanical properties of tissues, as well as its links with human disorders.
    Journal of Cell Science 09/2015; DOI:10.1242/jcs.169748
  • [Show abstract] [Hide abstract]
    ABSTRACT: Dexamethasone (Dex), a glucocorticoid drug, is often used to induce osteoblast commitment of mesenchymal stem cells (MSCs) that requires RhoA-dependent cellular tension. The underlying mechanism is unclear. In this study, we show that Dex stimulates expression of fibronectin (FN) and integrin α5 (ITGA5), accompanied by an increase in the interaction of GEF-H1 with Sec5, a microtubule (MT)-regulated RhoA activator and a component of exocyst, respectively. Disruption of this interaction abolishes Dex-induced cellular tension and GEF-H1 targeting to focal adhesion sites at cell periphery without affecting Dex-induced levels of ITGA5 and FN, while the extracellular deposit of FN to adhesion sites is specifically inhibited. We demonstrate that Dex stimulates the expression of serum/glucocorticoid-induced protein kinase 1 (SGK1), which is necessary and sufficient for the induction of Sec5/GEF-H1 interaction. Given the function of SGK1 in suppressing MT growth, our data suggest that the induction of SGK1 by Dex treatment alters MT dynamics to increase Sec5/GEF-H1 interaction, which promotes GEF-H1 targeting to adhesion sites. This mechanism is essential for the fibril formation of FN with integrin at adhesion sites that generates cellular tension.
    Journal of Cell Science 09/2015; DOI:10.1242/jcs.169961
  • [Show abstract] [Hide abstract]
    ABSTRACT: In many epithelial cells, epidermal growth factor (EGF) augments the epithelial-mesenchymal transition (EMT) that occurs when cells are treated with transforming growth factor beta (TGFβ). Here, we demonstrate that this augmentation requires activation of SH2 domain-containing phosphatase-2 (SHP2), a proto-oncogene. In lung and pancreatic cancer cell lines, reductions in E-cadherin expression, increases in vimentin expression, and increases in cell scatter rates were larger when cells were treated with TGFβ and EGF versus TGFβ or EGF alone. SHP2 knockdown promoted epithelial characteristics basally and antagonized EMT in response to TGFβ alone or in combination with EGF. Whereas EGF promoted SHP2 binding to tyrosine phosphorylated GAB1, which promotes SHP2 activity, TGFβ did not induce SHP2 association with phosphotyrosine-containing proteins. Knockdown of endogenous SHP2 and reconstitution with an SHP2 mutant with impaired phosphotyrosine binding ability eliminated the EGF-mediated EMT augmentation that was otherwise restored with wild-type SHP2 reconstitution. These results demonstrate roles for basal and ligand-induced SHP2 activity in EMT and further motivate efforts to identify specific ways to inhibit SHP2, given the role of EMT in tumor dissemination and chemoresistance.
    Journal of Cell Science 09/2015; DOI:10.1242/jcs.169599
  • [Show abstract] [Hide abstract]
    ABSTRACT: Cell surface adhesion receptors play diverse functions in multicellular development. In Dictyostelium, two immunoglobulin-like adhesion proteins, TgrB1 and TgrC1, are essential components with dual roles in morphogenesis and allorecognition during development. TgrB1 and TgrC1 form a heterophilic adhesion complex during cell contact and mediate intercellular communication. The underlying signaling pathways, however, have not been characterized. Here, we report on a mutation that suppresses the tgrB1/tgrC1-defective developmental arrest. The mutated gene alg9 encodes a putative mannosyl transferase that participates in N-linked protein glycosylation. We show that alteration in N-linked glycosylation, caused by alg9(ins) mutation or tunicamycin treatment, can partially suppress the developmental phenotypes caused by tgrC1 deletion or replacement with an incompatible allele. The alg9(ins) mutation also preferentially primed cells toward a stalk-cell fate. Despite its effect on development, we found that altered N-linked glycosylation had no discernable effect on TgrB1-TgrC1-mediated allorecognition. Our results show that N-linked protein glycosylation can modulate developmental processes without disturbing cell-cell recognition, suggesting that tgrB1 and tgrC1 have distinct effects in the two processes.
    Journal of Cell Science 09/2015; DOI:10.1242/jcs.172882
  • [Show abstract] [Hide abstract]
    ABSTRACT: We show here that the combination of an intracellular bi-partite calmodulin (CaM) binding site and a distant assembly region affects how an ion channel is regulated by a membrane lipid. Our data reveal that regulation by phosphatidylinositol(4,5)bisphosphate (PI(4,5)P2) and stabilization of assembled Kv7.2 subunits by intracellular coiled-coil regions far from the membrane are coupled molecular processes. Live cell fluorescence energy transfer measurements and direct binding studies indicate that remote coiled-coil formation creates conditions for different CaM interaction modes, each conferring different PI(4,5)P2 dependency to Kv7.2 channels. Disruption of coiled-coil formation by an epilepsy causing mutation decreases apparent CaM binding affinity and interrupts CaM influence on PI(4,5)P2 sensitivity.
    Journal of Cell Science 09/2015; DOI:10.1242/jcs.176420
  • [Show abstract] [Hide abstract]
    ABSTRACT: In higher eukaryotes, efficient chromosome congression relies, among other players, on the activity of chromokinesins. Here, we provide a quantitative analysis of kinetochore oscillations and positioning in S. Pombe, a model organism lacking chromokinesins. In wild type cells, chromosomes align during prophase and while oscillating, maintain this alignment throughout metaphase. Chromosome oscillations are dispensable both for kinetochore congression and stable kinetochore alignment during metaphase. In higher eukaryotes, Kinesin-8 controls chromosome congression by regulating their oscillations. Oppositely, we demonstrate that fission yeast Kinesin-8 controls chromosome congression by an alternative mechanism. We propose that Kinesin-8 aligns chromosomes by controlling pulling forces in a length dependent manner. A coarse grained model of chromosome segregation implemented with a length-dependent process that controls the force at kinetochores is necessary and sufficient to mimic kinetochore alignment and prevents the appearance of lagging chromosomes. Altogether, these data illustrate how the local action of a motor protein at kinetochores provides spatial cues within the spindle to align chromosomes and to prevent aneuploidy.
    Journal of Cell Science 09/2015; DOI:10.1242/jcs.160465
  • [Show abstract] [Hide abstract]
    ABSTRACT: Gap junctions formed of Cx36 show tremendous functional plasticity on several time scales. Changes in connexin phosphorylation modify coupling in minutes through an order of magnitude, but recent studies also imply involvement of connexin turnover in regulating cell-cell communication. We utilized Cx36 with an internal HaloTag to study Cx36 turnover and trafficking in cultured cells. Irreversible, covalent pulse-chase labeling with fluorescent HaloTag ligands allowed clear discrimination of newly formed and pre-existing Cx36. Cx36 in junctional plaques turned over with a half-life of 3.1 hours, and the turnover rate was unchanged by manipulations of PKA activity. In contrast, changes in PKA activity altered coupling within 20 minutes. New Cx36 in cargo vesicles was added directly to existing gap junctions and newly made Cx36 was not confined to points of addition, but diffused throughout existing gap junctions. Existing connexins also diffused into photobleached areas with a half-time of less than 2 seconds. In conclusion, studies of Cx36-HaloTag revealed novel features of connexin trafficking and demonstrated that phosphorylation-based changes in coupling occur on a different time scale than does turnover.
    Journal of Cell Science 09/2015; DOI:10.1242/jcs.162586
  • [Show abstract] [Hide abstract]
    ABSTRACT: Globoid cell leukodystrophy (Krabbe disease, KD) is a rare infantile neurodegenerative disorder. KD is caused by deficiency in the lysosomal enzyme galactocerebrosidase (GALC) resulting in brain accumulation, in the micromolar range, of the toxic metabolite galactosylsphingosine (psychosine). Here we find psychosine induces human astrocyte cell death likely via an apoptotic process in a concentration- and time-dependent manner (EC50 ∼15 µM at 4h). We show these effects of psychosine are attenuated by pre-treatment with the sphingosine 1-phosphate receptor agonist pFTY720 (Fingolimod) (IC50 ∼100nM). Psychosine (1 µM, 10 µM) also potentiates LPS-induced (EC50 ∼100ng/ml) production of pro-inflammatory cytokines in mouse astrocytes, which is also attenuated by pFTY720 (1 µM). Most notably, for the first time, we show that psychosine, at a concentration found in the brains of patients with KD (EC50 ∼100nM) directly induces demyelination in mouse organotypic cerebellar slices in a manner that is independent of proinflammatory cytokine response and that pFTY720 (0.1nM) significantly inhibits. These results support the idea that psychosine is a pathogenic agent in KD and suggest that sphingosine 1-phosphate signalling could be a potential drug target for this illness.
    Journal of Cell Science 09/2015; DOI:10.1242/jcs.169342
  • [Show abstract] [Hide abstract]
    ABSTRACT: Dynamic protein phosphorylation and dephosphorylation, mediated by a conserved cohort of protein kinases or phosphatases, regulate cell cycle progression. Among the well-known PP2A-like protein phosphatases, PP6 has been analyzed in mammalian mitosis recently identifying Aurora A as its key substrate. However, the functions of PP6 in meiosis are still entirely unknown. To identify the physiological role of PP6 in female gametogenesis, Ppp6c(F/F) mice were first generated and crossed with Zp3-Cre mice to selectively disrupt Ppp6c expression in oocytes. Here we report for the first time that PP6c was dispensable for oocyte meiotic maturation but essential for MII exit after fertilization, since depletion of PP6c caused abnormal MII spindle and disrupted MII cytokinesis, resulting in zygotes with high risk of aneuploidy, defective early embryonic development, thus severe subfertility. We also revealed that PP6 inactivation interfered with MII spindle formation and MII exit due to increased Aurora A activity, and Aurora A inhibition with MLN8237 could rescue the PP6c depletion phenotype. In conclusion, our findings uncover a hitherto unknown role for PP6 as an indispensable regulator of oocyte meiosis and female fertility.
    Journal of Cell Science 09/2015; DOI:10.1242/jcs.173179
  • [Show abstract] [Hide abstract]
    ABSTRACT: Selectins facilitate the recruitment of circulating cells from the bloodstream by mediating rolling adhesion, which initiates the cell-cell signaling that directs extravasation into surrounding tissues. To measure the relative efficiency of cell adhesion in shear flow for in vitro drug screening, we designed and implemented a microfluidic-based analytical cell adhesion chromatography system. The juxtaposition of instantaneous rolling velocities with elution times revealed that human metastatic cancer cells but not human leukocytes have a reduced capacity to sustain rolling adhesion with P-selectin. We define a new parameter, termed adhesion persistence, which is conceptually similar to migration persistence in the context of chemotaxis but instead describes the capacity of cells to resist the influence of shear flow and sustain rolling interactions with an adhesive substrate that may modulate the probability of extravasation. Among cell types assayed, adhesion persistence to P-selectin is specifically reduced in metastatic but not leukocyte-like cells in response to low-dose heparin. In conclusion, we demonstrate this as an effective methodology to identify selectin adhesion antagonist doses that modulate homing cell adhesion and engraftment in a cell subtype-selective manner.
    Journal of Cell Science 09/2015; DOI:10.1242/jcs.166439