The research report should be a detailed narrative explaining the function, biological processes, and localization of the gene product. Citations should be given for all claims.
You should prioritize authoritative reviews and primary scientific literature when conducting research. You can supplement
this with annotations you find in gene/protein databases, but these can be outdated or inaccurate.
We are specifically interested in the primary function of the gene - for enzymes, what reaction is catalyzed, and what is the substrate specificity? For transporters, what is the substrate? For structural proteins or adapters, what is the broader structural role? For signaling molecules, what is the role in the pathway.
We are interested in where in or outside the cell the gene product carries out its function.
We are also interested in the signaling or biochemical pathways in which the gene functions. We are less interested in broad pleiotropic effects, except where these elucidate the precise role.
Include evidence where possible. We are interested in both experimental evidence as well as inference from structure, evolution, or bioinformatic analysis. Precise studies should be prioritized over high-throughput, where available.
The C. elegans gene mcm-4 (historically lin-6; UniProt lists additional synonyms including let-358) encodes the MCM4 subunit of the conserved MCM2–7 replicative helicase/replication-licensing machinery, a core component required to license DNA replication origins and (after activation as CMG) unwind DNA during S phase. In worms, loss of mcm-4 uncouples cell-cycle progression from DNA synthesis (mitosis can proceed despite failed replication), reveals roles in replication checkpoint signaling, and shows strong tissue-specific requirements—particularly in the epidermis for organismal growth and viability. Recent 2023–2024 structural and mechanistic work across eukaryotes has clarified how loaded MCM double hexamers are activated into CMG to melt/unwind origins, and 2024 C. elegans genetics provides evidence that the CMG complex can also influence cell-fate divergence via chromatin/histone-inheritance mechanisms, highlighting potential noncanonical functions of MCM-containing assemblies.
Primary C. elegans genetics explicitly establishes that the historical locus lin-6 corresponds to mcm-4 and encodes the single C. elegans MCM-4 subunit of the MCM2–7 replicative helicase, within the replication pre-initiation/licensing machinery. (korzelius2011c.elegansmcm4 pages 4-5, korzelius2011c.elegansmcm4 pages 9-9, korzelius2011c.elegansmcm4 pages 1-2)
Important scope note. The retrieved primary literature directly supports the mcm-4 ↔ lin-6 ↔ MCM4-ortholog mapping in C. elegans, but it does not explicitly mention the UniProt accession Q95XQ8 or the synonym let-358 in the excerpted sections available here; those identifiers are therefore treated as database-provided context rather than paper-verified in this report. (korzelius2011c.elegansmcm4 pages 2-3, korzelius2011c.elegansmcm4 pages 4-5)
MCM-4 is not typically a standalone enzyme; rather, it contributes as one subunit to the enzymatic activities of the MCM2–7/CMG helicase. MCM proteins carry ATP-binding motifs and are attributed ATPase and helicase activities, with ATP hydrolysis within the MCM ring driving DNA translocation and unwinding in CMG. (you2024assemblyactivationand pages 2-4, xiang2023thecmghelicase pages 4-6)
A widely used biochemical dissection highlights that an MCM4/6/7 subcomplex exhibits intrinsic ssDNA-dependent ATP hydrolysis and 3′→5′ helicase activity, with preferences for forked/bubble DNA structures and certain ssDNA contexts (e.g., T-rich ssDNA activating activity). This informs substrate and polarity expectations for MCM4-containing helicase action in vivo. (you2024assemblyactivationand pages 2-4)
At the replication fork, the activated CMG helicase translocates 3′→5′ on the leading-strand ssDNA template while unwinding parental duplex DNA, thereby providing ssDNA templates for polymerases. (xiang2023thecmghelicase pages 4-6, xu2023synergismbetweencmg pages 1-2)
In vivo, the full MCM2–7 heterohexamer is required for replication licensing and for initiation/elongation; activation into CMG occurs via kinase-driven recruitment of firing factors and accessory proteins. (you2024assemblyactivationand pages 1-2, you2024assemblyactivationand pages 4-6)
In C. elegans, mcm-4/lin-6 is required for DNA synthesis in multiple somatic lineages; mutants can enter the G1/S transition but fail to replicate DNA in most postembryonic lineages. (korzelius2011c.elegansmcm4 pages 4-5, korzelius2011c.elegansmcm4 pages 1-2)
The cell-cycle timing and localization of MCM-4 support a licensing role: MCM-4 associates with chromatin in late anaphase (a conserved licensing window at mitotic exit) and is strongly induced around S-phase onset in cycling lineages. (korzelius2011c.elegansmcm4 pages 9-11, korzelius2011c.elegansmcm4 pages 9-9)
Worm experiments support that MCM-4 contributes to replication checkpoint responses: embryos depleted of MCM components can show absence of DNA replication with continued mitotic DNA segregation and genome fragmentation, consistent with defective coupling between replication completion and mitotic entry. (korzelius2011c.elegansmcm4 pages 5-7)
Moreover, MCM-4 perturbation can reduce a replication-stress-induced delay of mitotic progression (e.g., in contexts of nucleotide depletion), consistent with MCM-dependent generation of ssDNA at stalled forks that enables checkpoint signaling (ATR/CHK-1 pathway logic discussed in the worm study). (korzelius2011c.elegansmcm4 pages 5-7, korzelius2011c.elegansmcm4 pages 9-11)
Despite being a core replication factor, mcm-4 shows a striking tissue-specific requirement for animal growth and viability. Epidermal expression of MCM-4 (Pdpy-7-driven) restores larval growth and viability in mcm-4 mutants, whereas intestine-specific expression rescues intestinal nuclear divisions/endoreduplication but not organismal viability. (korzelius2011c.elegansmcm4 pages 9-9, korzelius2011c.elegansmcm4 pages 9-11)
MCM-4 acts in the nucleus/chromatin compartment consistent with its licensing/helicase roles. In C. elegans, MCM-4 is nuclear during interphase, becomes diffuse upon nuclear envelope breakdown and is not associated with metaphase chromatin, and then reassociates with chromatin in late anaphase, consistent with re-licensing at mitotic exit. (korzelius2011c.elegansmcm4 pages 9-9, ruijtenberg2011regulationofdna pages 3-6, korzelius2011c.elegansmcm4 pages 5-7)
Live-embryo imaging of other MCM2–7 subunits (e.g., GFP–MCM-2/3) demonstrates that chromatin association during late M phase depends on pre-RC factors (CDC-6, CDT-1, ORC) and that nuclear accumulation can include a large soluble pool during interphase. This supports the conserved model that MCM chromatin loading is temporally regulated and tightly controlled to prevent rereplication. (sonneville2012thedynamicsof pages 2-4, sonneville2012thedynamicsof pages 1-2)
Visual support. Key images from Korzelius et al. (2011) show MCM-4 localization dynamics (Figures 5–6) and epidermal rescue (Figure 7). (korzelius2011c.elegansmcm4 media d50caf5d, korzelius2011c.elegansmcm4 media a6161eb6, korzelius2011c.elegansmcm4 media 9b7439f9)
A 2024 cryo-EM reconstitution study visualized staged origin unwinding: firing factors assemble on the MCM double hexamer to nucleate DNA melting, with quantifiable initial distortion (reported as ~0.7 turns untwisted and ≥3 bp broken in early intermediates), and Mcm10 then triggers splitting into two helicases and lagging-strand ejection to form productive forks. (henrikus2024unwindingofa pages 1-2)
A 2024 review synthesizes biochemical and structural data supporting steric-exclusion unwinding, highlighting kinase regulation (DDK/CDK) and stepwise recruitment of Cdc45/GINS to form active CMG. (you2024assemblyactivationand pages 1-2, you2024assemblyactivationand pages 6-7)
A 2023 Nature Communications structural study further emphasizes ordered kinase-dependent assembly and the coupling between CMG and leading-strand polymerase Polε, describing ATPase-site rearrangements and dynamic polymerase engagement that coordinates unwinding and synthesis. (xu2023synergismbetweencmg pages 1-2)
A 2024 C. elegans Nature Communications study reports that the CMG helicase complex (studying GINS subunit PSF-2) is required for divergence of daughter fates during asymmetric divisions, including transcriptional upregulation of the pro-apoptotic gene egl-1. The authors propose a mechanism separable from DNA unwinding, implicating replication-coupled chromatin/histone-handling activities (histone chaperone-like effects) that produce epigenetic changes at the egl-1 locus during mother-cell replication. Quantitative results include: the worm soma produces 1090 somatic cells with 131 deaths, apoptosis occurs ~20–30 min after terminal division, and psf-2 perturbation blocks specific programmed deaths (e.g., 67% of MSpaapp deaths blocked) and disrupts egl-1 mRNA asymmetry measured by single-molecule RNA FISH. (memar2024thereplicativehelicase pages 1-2, memar2024thereplicativehelicase pages 8-9)
Although this is not mcm-4-specific, it is highly relevant context because MCM-4 is an obligate CMG core subunit; thus the study motivates careful consideration of potential beyond-replication roles for CMG/MCM assemblies in worm development. (memar2024thereplicativehelicase pages 1-2, memar2024thereplicativehelicase pages 10-11)
A 2024 Molecular Cancer Therapeutics study identified ATP-competitive inhibitors of human CMG/MCM ATPase/helicase activity (amino-coumarins clorobiocin and coumermycin-A1) that disrupt ATP-dependent CMG assembly steps (e.g., MCM ring assembly and GINS recruitment) and destabilize replisome components, inducing DNA damage and selective toxicity in K-Ras mutant tumor cells. This is a concrete example of “real-world implementation” of mechanistic MCM research in drug discovery. (xiang2024identificationofatpcompetitive pages 1-2)
Worm studies have implemented MCM-4::mCherry reporters (including MosSCI single-copy rescue constructs) to visualize cell-cycle regulated localization and to validate functional rescue of mcm-4 null mutants. (ruijtenberg2011regulationofdna pages 1-3, ruijtenberg2011regulationofdna pages 3-6)
A 2017 PLoS ONE paper developed a live reporter for cell-cycle entry that combines the mcm-4 promoter (as a readout of Rb/E2F-mediated transcriptional control) with a CDK-activity sensor to mark cell-cycle commitment in seam cells—illustrating practical use of mcm-4 regulatory sequences as a proliferation/cell-cycle marker. (xiang2024identificationofatpcompetitive pages 1-2)
Worm replication studies use EdU/BrdU incorporation, DNA-content quantification by confocal serial sections, and flow cytometry of dissociated cells with GFP gating to analyze replication and cell-cycle states in specific tissues. (ruijtenberg2011regulationofdna pages 3-6)
The C. elegans mcm-4 literature indicates a general replication/helicase role but a particularly strong epidermal requirement for growth/viability (rescuable by epidermal expression). A plausible expert interpretation (consistent with licensing theory) is that tissues differ in replication demand, tolerance to replication stress, reliance on dormant origins, and checkpoint robustness; in such a model, an epidermal lineage could be more sensitive to reduced licensing/helicase capacity. This interpretation aligns with the broader licensing framework where excess loaded MCM supports dormant origins under stress and replication completion. (korzelius2011c.elegansmcm4 pages 9-9, korzelius2011c.elegansmcm4 pages 9-11, you2024assemblyactivationand pages 1-2)
The 2024 finding that CMG (via GINS subunit PSF-2) can influence fate divergence through a mechanism proposed to be independent of unwinding suggests that MCM-containing replisome components may contribute to chromatin-state inheritance and gene-expression competence. For mcm-4 annotation, the strongest evidence remains canonical licensing/helicase roles, but functional annotation should remain open to CMG-dependent chromatin regulation in specific developmental contexts. (memar2024thereplicativehelicase pages 1-2, memar2024thereplicativehelicase pages 10-11, memar2024thereplicativehelicase pages 8-9)
The following table consolidates the main findings, explicitly separating worm primary evidence from cross-species mechanistic inference and listing quantitative datapoints.
| Topic | Key findings | Evidence type (worm primary vs cross-species review/structural) | Best supporting sources (authors, year, URL) | Citation IDs to use |
|---|---|---|---|---|
| Identity / synonyms | The target is Caenorhabditis elegans mcm-4, historically identified as lin-6; primary worm literature states that lin-6 corresponds to mcm-4 and encodes the single C. elegans MCM-4 subunit of the MCM2-7 replicative helicase / replication licensing machinery. UniProt-provided synonyms also include let-358; this synonym was not explicitly recovered in the retrieved papers, so it should be treated as database-supported rather than paper-verified here. | Worm primary + database-context alignment | Korzelius et al., 2011, https://doi.org/10.1016/j.ydbio.2010.12.009; Ruijtenberg et al., 2011, https://doi.org/10.5772/19397 | (korzelius2011c.elegansmcm4 pages 2-3, korzelius2011c.elegansmcm4 pages 4-5, korzelius2011c.elegansmcm4 pages 9-9, ruijtenberg2011regulationofdna pages 3-6) |
| Molecular function | MCM-4 functions as one subunit of the AAA+ ATPase MCM2-7 heterohexamer, the core of the eukaryotic replicative helicase. In active form, CMG (Cdc45-MCM2-7-GINS) uses ATP hydrolysis to unwind parental duplex DNA by steric exclusion while translocating 3'→5' on the leading-strand ssDNA. Substrate context: dsDNA at licensed origins is converted to ssDNA templates for replication forks; MCM4 contributes to this complex activity rather than acting as a known standalone enzyme in worms. | Cross-species review/structural, used to infer precise biochemistry for worm ortholog | You & Masai, 2024, https://doi.org/10.3390/biology13080629; Xu et al., 2023, https://doi.org/10.1038/s41467-023-41506-0; Xiang et al., 2023, https://doi.org/10.1038/s41388-022-02572-8 | (you2024assemblyactivationand pages 2-4, you2024assemblyactivationand pages 1-2, you2024assemblyactivationand pages 4-6, xiang2023thecmghelicase pages 4-6, xu2023synergismbetweencmg pages 1-2) |
| Biological processes / pathways | Core role in replication licensing, origin firing, S-phase progression, and the replication checkpoint. In worms, mcm-4 is required for productive DNA synthesis and contributes to checkpoint-dependent delay of mitosis under replication stress; it acts in the conserved pathway with ORC, CDC-6, CDT-1, and downstream CMG assembly/activation factors. | Worm primary with mechanistic support from reviews | Korzelius et al., 2011, https://doi.org/10.1016/j.ydbio.2010.12.009; Sonneville et al., 2012, https://doi.org/10.1083/jcb.201110080; Gaggioli et al., 2014, https://doi.org/10.1083/jcb.201310083; You & Masai, 2024, https://doi.org/10.3390/biology13080629 | (korzelius2011c.elegansmcm4 pages 5-7, korzelius2011c.elegansmcm4 pages 9-11, ruijtenberg2011regulationofdna pages 3-6, sonneville2012thedynamicsof pages 2-4, sonneville2012thedynamicsof pages 1-2, sonneville2012thedynamicsof pages 4-6) |
| Localization / dynamics | In C. elegans, MCM-4 is nuclear during interphase, diffuse / not chromosome-associated in metaphase, and re-associates with chromatin in late anaphase, matching licensing at mitotic exit. Related worm imaging of MCM2-7 shows loading in late M / early G1, with a large soluble nuclear pool in interphase and pre-RC dependence on cdc-6/cdt-1/orc-5. | Worm primary | Korzelius et al., 2011, https://doi.org/10.1016/j.ydbio.2010.12.009; Sonneville et al., 2012, https://doi.org/10.1083/jcb.201110080; Sonneville et al., 2015, https://doi.org/10.1016/j.celrep.2015.06.046 | (sonneville2012thedynamicsof pages 2-4, korzelius2011c.elegansmcm4 pages 9-9, ruijtenberg2011regulationofdna pages 3-6, korzelius2011c.elegansmcm4 pages 5-7, sonneville2015bothchromosomedecondensation pages 1-3, korzelius2011c.elegansmcm4 pages 1-2) |
| Key phenotypes | Loss of mcm-4 causes failure of DNA replication with continued mitotic chromosome segregation, genome fragmentation, and defective checkpoint responses. Postembryonic somatic lineages are strongly affected, while gonad/germline can continue divisions longer, likely due to maternal product and stronger checkpoint buffering. | Worm primary | Korzelius et al., 2011, https://doi.org/10.1016/j.ydbio.2010.12.009 | (korzelius2011c.elegansmcm4 pages 5-7, korzelius2011c.elegansmcm4 pages 7-9, korzelius2011c.elegansmcm4 pages 4-5, korzelius2011c.elegansmcm4 pages 1-2) |
| Tissue-specific requirements | Although mcm-4 has a general replication role, worm experiments show an epidermis-specific requirement for organismal growth and viability. Pdpy-7::MCM-4::mCherry rescues larval growth and viability, while intestine-specific expression rescues intestinal nuclear divisions/endoreduplication but not whole-animal viability. This indicates strong tissue-specific sensitivity despite conserved core function. | Worm primary | Korzelius et al., 2011, https://doi.org/10.1016/j.ydbio.2010.12.009 | (korzelius2011c.elegansmcm4 pages 9-9, korzelius2011c.elegansmcm4 pages 9-11) |
| Replication-independent / beyond-replication roles | Recent C. elegans work on CMG, though centered on PSF-2/GINS2 rather than mcm-4 directly, shows that the replicative helicase can influence asymmetric cell-fate divergence and egl-1 transcription through a proposed histone-chaperone / chromatin inheritance mechanism that is separable from bulk DNA unwinding. This is relevant for interpreting potential noncanonical roles of MCM4-containing CMG in worms. | Worm primary (complex-level inference, not mcm-4-specific) | Memar et al., 2024, https://doi.org/10.1038/s41467-024-53715-2; Rankin & Rankin, 2024, https://doi.org/10.3390/biology13040258 | (memar2024thereplicativehelicase pages 1-2, memar2024thereplicativehelicase pages 11-12, memar2024thereplicativehelicase pages 10-11, memar2024thereplicativehelicase pages 9-10, memar2024thereplicativehelicase pages 8-9) |
| Recent structural/mechanistic developments (2023-2024) | 2023-2024 studies sharpen the mechanism of MCM activation: loaded double hexamers are converted into active CMG by DDK/CDK-dependent phosphorylation, recruitment of Cdc45/GINS/Polε, and Mcm10-triggered helicase splitting/origin melting. Cryo-EM visualized local origin unwinding, including ~0.7 turns untwisted and ≥3 bp broken in early activation intermediates. | Cross-species primary structural + review | Henrikus et al., 2024, https://doi.org/10.1038/s41594-024-01280-z; You & Masai, 2024, https://doi.org/10.3390/biology13080629; Weissmann et al., 2024, https://doi.org/10.1038/s41586-024-08263-6 | (you2024assemblyactivationand pages 1-2, henrikus2024unwindingofa pages 1-2, you2024assemblyactivationand pages 6-7) |
| Applications / real-world implementations | In worms, MCM-4 promoter/reporters are used as practical cell-cycle entry and proliferation markers; live MCM-4::mCherry supports lineage-level imaging of licensing dynamics. More broadly, the CMG/MCM ATPase has become a tractable intervention point: 2024 work identified ATP-competitive CMG/MCM inhibitors (e.g., clorobiocin, coumermycin-A1) that disrupt helicase assembly and fork function, illustrating translational relevance of the MCM4-containing complex. | Worm tool + cross-species therapeutic application | van Rijnberk et al., 2017, https://doi.org/10.1371/journal.pone.0171600; Ruijtenberg et al., 2011, https://doi.org/10.5772/19397; Xiang et al., 2024, https://doi.org/10.1158/1535-7163.mct-23-0904 | (ruijtenberg2011regulationofdna pages 3-6, xiang2024identificationofatpcompetitive pages 1-2) |
| Key quantitative / statistical data points | MCM-4 protein predicted at 823 aa in C. elegans. In structural activation intermediates, origin DNA is untwisted by ~0.7 turns with at least 3 bp broken. In the 2024 CMG fate-divergence study, the C. elegans soma produces 1090 somatic cells, 131 die, and apoptosis occurs ~20–30 min after terminal division; in psf-2(t3443ts), 67% of MSpaapp deaths were blocked and AMso fate defects reached 82% (167/204) among divisions scored. | Mixed: worm primary + cross-species structural + worm primary beyond-replication | Korzelius et al., 2011, https://doi.org/10.1016/j.ydbio.2010.12.009; Henrikus et al., 2024, https://doi.org/10.1038/s41594-024-01280-z; Memar et al., 2024, https://doi.org/10.1038/s41467-024-53715-2 | (korzelius2011c.elegansmcm4 pages 2-3, henrikus2024unwindingofa pages 1-2, memar2024thereplicativehelicase pages 1-2, memar2024thereplicativehelicase pages 9-10, memar2024thereplicativehelicase pages 8-9) |
Table: This table condenses the most relevant identity, function, localization, phenotype, and recent mechanistic findings for C. elegans mcm-4/lin-6. It separates direct worm evidence from cross-species mechanistic inference and provides citation IDs for efficient reuse in the final report.
References
(korzelius2011c.elegansmcm4 pages 4-5): Jerome Korzelius, Inge The, Suzan Ruijtenberg, Vincent Portegijs, Huihong Xu, H. Robert Horvitz, and Sander van den Heuvel. C. elegans mcm-4 is a general dna replication and checkpoint component with an epidermis-specific requirement for growth and viability. Developmental Biology, 350:358-369, Feb 2011. URL: https://doi.org/10.1016/j.ydbio.2010.12.009, doi:10.1016/j.ydbio.2010.12.009. This article has 32 citations and is from a peer-reviewed journal.
(korzelius2011c.elegansmcm4 pages 9-9): Jerome Korzelius, Inge The, Suzan Ruijtenberg, Vincent Portegijs, Huihong Xu, H. Robert Horvitz, and Sander van den Heuvel. C. elegans mcm-4 is a general dna replication and checkpoint component with an epidermis-specific requirement for growth and viability. Developmental Biology, 350:358-369, Feb 2011. URL: https://doi.org/10.1016/j.ydbio.2010.12.009, doi:10.1016/j.ydbio.2010.12.009. This article has 32 citations and is from a peer-reviewed journal.
(korzelius2011c.elegansmcm4 pages 1-2): Jerome Korzelius, Inge The, Suzan Ruijtenberg, Vincent Portegijs, Huihong Xu, H. Robert Horvitz, and Sander van den Heuvel. C. elegans mcm-4 is a general dna replication and checkpoint component with an epidermis-specific requirement for growth and viability. Developmental Biology, 350:358-369, Feb 2011. URL: https://doi.org/10.1016/j.ydbio.2010.12.009, doi:10.1016/j.ydbio.2010.12.009. This article has 32 citations and is from a peer-reviewed journal.
(korzelius2011c.elegansmcm4 pages 2-3): Jerome Korzelius, Inge The, Suzan Ruijtenberg, Vincent Portegijs, Huihong Xu, H. Robert Horvitz, and Sander van den Heuvel. C. elegans mcm-4 is a general dna replication and checkpoint component with an epidermis-specific requirement for growth and viability. Developmental Biology, 350:358-369, Feb 2011. URL: https://doi.org/10.1016/j.ydbio.2010.12.009, doi:10.1016/j.ydbio.2010.12.009. This article has 32 citations and is from a peer-reviewed journal.
(you2024assemblyactivationand pages 1-2): Zhiying You and Hisao Masai. Assembly, activation, and helicase actions of mcm2-7: transition from inactive mcm2-7 double hexamers to active replication forks. Biology, 13:629, Aug 2024. URL: https://doi.org/10.3390/biology13080629, doi:10.3390/biology13080629. This article has 9 citations.
(you2024assemblyactivationand pages 4-6): Zhiying You and Hisao Masai. Assembly, activation, and helicase actions of mcm2-7: transition from inactive mcm2-7 double hexamers to active replication forks. Biology, 13:629, Aug 2024. URL: https://doi.org/10.3390/biology13080629, doi:10.3390/biology13080629. This article has 9 citations.
(henrikus2024unwindingofa pages 1-2): Sarah S. Henrikus, Marta H. Gross, Oliver Willhoft, Thomas Pühringer, Jacob S. Lewis, Allison W. McClure, Julia F. Greiwe, Giacomo Palm, Andrea Nans, John F. X. Diffley, and Alessandro Costa. Unwinding of a eukaryotic origin of replication visualized by cryo-em. Nature Structural & Molecular Biology, 31:1265-1276, May 2024. URL: https://doi.org/10.1038/s41594-024-01280-z, doi:10.1038/s41594-024-01280-z. This article has 32 citations and is from a highest quality peer-reviewed journal.
(xiang2023thecmghelicase pages 4-6): Shengyan Xiang, Damon R. Reed, and Mark G. Alexandrow. The cmg helicase and cancer: a tumor “engine” and weakness with missing mutations. Oncogene, 42:473-490, Dec 2023. URL: https://doi.org/10.1038/s41388-022-02572-8, doi:10.1038/s41388-022-02572-8. This article has 31 citations and is from a domain leading peer-reviewed journal.
(you2024assemblyactivationand pages 2-4): Zhiying You and Hisao Masai. Assembly, activation, and helicase actions of mcm2-7: transition from inactive mcm2-7 double hexamers to active replication forks. Biology, 13:629, Aug 2024. URL: https://doi.org/10.3390/biology13080629, doi:10.3390/biology13080629. This article has 9 citations.
(xu2023synergismbetweencmg pages 1-2): Zhichun Xu, Jianrong Feng, Daqi Yu, Yunjing Huo, Xiaohui Ma, Wai Hei Lam, Zheng Liu, Xiang David Li, Toyotaka Ishibashi, Shangyu Dang, and Yuanliang Zhai. Synergism between cmg helicase and leading strand dna polymerase at replication fork. Nature Communications, Sep 2023. URL: https://doi.org/10.1038/s41467-023-41506-0, doi:10.1038/s41467-023-41506-0. This article has 34 citations and is from a highest quality peer-reviewed journal.
(korzelius2011c.elegansmcm4 pages 9-11): Jerome Korzelius, Inge The, Suzan Ruijtenberg, Vincent Portegijs, Huihong Xu, H. Robert Horvitz, and Sander van den Heuvel. C. elegans mcm-4 is a general dna replication and checkpoint component with an epidermis-specific requirement for growth and viability. Developmental Biology, 350:358-369, Feb 2011. URL: https://doi.org/10.1016/j.ydbio.2010.12.009, doi:10.1016/j.ydbio.2010.12.009. This article has 32 citations and is from a peer-reviewed journal.
(korzelius2011c.elegansmcm4 pages 5-7): Jerome Korzelius, Inge The, Suzan Ruijtenberg, Vincent Portegijs, Huihong Xu, H. Robert Horvitz, and Sander van den Heuvel. C. elegans mcm-4 is a general dna replication and checkpoint component with an epidermis-specific requirement for growth and viability. Developmental Biology, 350:358-369, Feb 2011. URL: https://doi.org/10.1016/j.ydbio.2010.12.009, doi:10.1016/j.ydbio.2010.12.009. This article has 32 citations and is from a peer-reviewed journal.
(ruijtenberg2011regulationofdna pages 3-6): Suzan Ruijtenberg, Sander van den Heuvel, and Inge The. Regulation of dna synthesis and replication checkpoint activation during c. elegans development. ArXiv, Sep 2011. URL: https://doi.org/10.5772/19397, doi:10.5772/19397. This article has 1 citations.
(sonneville2012thedynamicsof pages 2-4): Remi Sonneville, Matthieu Querenet, Ashley Craig, Anton Gartner, and J. Julian Blow. The dynamics of replication licensing in live caenorhabditis elegans embryos. The Journal of Cell Biology, 196:233-246, Jan 2012. URL: https://doi.org/10.1083/jcb.201110080, doi:10.1083/jcb.201110080. This article has 88 citations.
(sonneville2012thedynamicsof pages 1-2): Remi Sonneville, Matthieu Querenet, Ashley Craig, Anton Gartner, and J. Julian Blow. The dynamics of replication licensing in live caenorhabditis elegans embryos. The Journal of Cell Biology, 196:233-246, Jan 2012. URL: https://doi.org/10.1083/jcb.201110080, doi:10.1083/jcb.201110080. This article has 88 citations.
(korzelius2011c.elegansmcm4 media d50caf5d): Jerome Korzelius, Inge The, Suzan Ruijtenberg, Vincent Portegijs, Huihong Xu, H. Robert Horvitz, and Sander van den Heuvel. C. elegans mcm-4 is a general dna replication and checkpoint component with an epidermis-specific requirement for growth and viability. Developmental Biology, 350:358-369, Feb 2011. URL: https://doi.org/10.1016/j.ydbio.2010.12.009, doi:10.1016/j.ydbio.2010.12.009. This article has 32 citations and is from a peer-reviewed journal.
(korzelius2011c.elegansmcm4 media a6161eb6): Jerome Korzelius, Inge The, Suzan Ruijtenberg, Vincent Portegijs, Huihong Xu, H. Robert Horvitz, and Sander van den Heuvel. C. elegans mcm-4 is a general dna replication and checkpoint component with an epidermis-specific requirement for growth and viability. Developmental Biology, 350:358-369, Feb 2011. URL: https://doi.org/10.1016/j.ydbio.2010.12.009, doi:10.1016/j.ydbio.2010.12.009. This article has 32 citations and is from a peer-reviewed journal.
(korzelius2011c.elegansmcm4 media 9b7439f9): Jerome Korzelius, Inge The, Suzan Ruijtenberg, Vincent Portegijs, Huihong Xu, H. Robert Horvitz, and Sander van den Heuvel. C. elegans mcm-4 is a general dna replication and checkpoint component with an epidermis-specific requirement for growth and viability. Developmental Biology, 350:358-369, Feb 2011. URL: https://doi.org/10.1016/j.ydbio.2010.12.009, doi:10.1016/j.ydbio.2010.12.009. This article has 32 citations and is from a peer-reviewed journal.
(you2024assemblyactivationand pages 6-7): Zhiying You and Hisao Masai. Assembly, activation, and helicase actions of mcm2-7: transition from inactive mcm2-7 double hexamers to active replication forks. Biology, 13:629, Aug 2024. URL: https://doi.org/10.3390/biology13080629, doi:10.3390/biology13080629. This article has 9 citations.
(memar2024thereplicativehelicase pages 1-2): Nadin Memar, Ryan Sherrard, Aditya Sethi, Carla Lloret Fernandez, Henning Schmidt, Eric J. Lambie, Richard J. Poole, Ralf Schnabel, and Barbara Conradt. The replicative helicase cmg is required for the divergence of cell fates during asymmetric cell division in vivo. Nature Communications, Oct 2024. URL: https://doi.org/10.1038/s41467-024-53715-2, doi:10.1038/s41467-024-53715-2. This article has 7 citations and is from a highest quality peer-reviewed journal.
(memar2024thereplicativehelicase pages 8-9): Nadin Memar, Ryan Sherrard, Aditya Sethi, Carla Lloret Fernandez, Henning Schmidt, Eric J. Lambie, Richard J. Poole, Ralf Schnabel, and Barbara Conradt. The replicative helicase cmg is required for the divergence of cell fates during asymmetric cell division in vivo. Nature Communications, Oct 2024. URL: https://doi.org/10.1038/s41467-024-53715-2, doi:10.1038/s41467-024-53715-2. This article has 7 citations and is from a highest quality peer-reviewed journal.
(memar2024thereplicativehelicase pages 10-11): Nadin Memar, Ryan Sherrard, Aditya Sethi, Carla Lloret Fernandez, Henning Schmidt, Eric J. Lambie, Richard J. Poole, Ralf Schnabel, and Barbara Conradt. The replicative helicase cmg is required for the divergence of cell fates during asymmetric cell division in vivo. Nature Communications, Oct 2024. URL: https://doi.org/10.1038/s41467-024-53715-2, doi:10.1038/s41467-024-53715-2. This article has 7 citations and is from a highest quality peer-reviewed journal.
(xiang2024identificationofatpcompetitive pages 1-2): Shengyan Xiang, Kendall C. Craig, Xingju Luo, Darcy L. Welch, Renan B. Ferreira, Harshani R. Lawrence, Nicholas J. Lawrence, Damon R. Reed, and Mark G. Alexandrow. Identification of atp-competitive human cmg helicase inhibitors for cancer intervention that disrupt cmg-replisome function. Molecular Cancer Therapeutics, 23:1568-1585, Jul 2024. URL: https://doi.org/10.1158/1535-7163.mct-23-0904, doi:10.1158/1535-7163.mct-23-0904. This article has 8 citations and is from a peer-reviewed journal.
(ruijtenberg2011regulationofdna pages 1-3): Suzan Ruijtenberg, Sander van den Heuvel, and Inge The. Regulation of dna synthesis and replication checkpoint activation during c. elegans development. ArXiv, Sep 2011. URL: https://doi.org/10.5772/19397, doi:10.5772/19397. This article has 1 citations.
(sonneville2012thedynamicsof pages 4-6): Remi Sonneville, Matthieu Querenet, Ashley Craig, Anton Gartner, and J. Julian Blow. The dynamics of replication licensing in live caenorhabditis elegans embryos. The Journal of Cell Biology, 196:233-246, Jan 2012. URL: https://doi.org/10.1083/jcb.201110080, doi:10.1083/jcb.201110080. This article has 88 citations.
(sonneville2015bothchromosomedecondensation pages 1-3): Remi Sonneville, Gillian Craig, Karim Labib, Anton Gartner, and J. Julian Blow. Both chromosome decondensation and condensation are dependent on dna replication in c. elegans embryos. Cell Reports, 12:405-417, Jul 2015. URL: https://doi.org/10.1016/j.celrep.2015.06.046, doi:10.1016/j.celrep.2015.06.046. This article has 44 citations and is from a highest quality peer-reviewed journal.
(korzelius2011c.elegansmcm4 pages 7-9): Jerome Korzelius, Inge The, Suzan Ruijtenberg, Vincent Portegijs, Huihong Xu, H. Robert Horvitz, and Sander van den Heuvel. C. elegans mcm-4 is a general dna replication and checkpoint component with an epidermis-specific requirement for growth and viability. Developmental Biology, 350:358-369, Feb 2011. URL: https://doi.org/10.1016/j.ydbio.2010.12.009, doi:10.1016/j.ydbio.2010.12.009. This article has 32 citations and is from a peer-reviewed journal.
(memar2024thereplicativehelicase pages 11-12): Nadin Memar, Ryan Sherrard, Aditya Sethi, Carla Lloret Fernandez, Henning Schmidt, Eric J. Lambie, Richard J. Poole, Ralf Schnabel, and Barbara Conradt. The replicative helicase cmg is required for the divergence of cell fates during asymmetric cell division in vivo. Nature Communications, Oct 2024. URL: https://doi.org/10.1038/s41467-024-53715-2, doi:10.1038/s41467-024-53715-2. This article has 7 citations and is from a highest quality peer-reviewed journal.
(memar2024thereplicativehelicase pages 9-10): Nadin Memar, Ryan Sherrard, Aditya Sethi, Carla Lloret Fernandez, Henning Schmidt, Eric J. Lambie, Richard J. Poole, Ralf Schnabel, and Barbara Conradt. The replicative helicase cmg is required for the divergence of cell fates during asymmetric cell division in vivo. Nature Communications, Oct 2024. URL: https://doi.org/10.1038/s41467-024-53715-2, doi:10.1038/s41467-024-53715-2. This article has 7 citations and is from a highest quality peer-reviewed journal.