About

Jean Cook, PhD, is a Professor of Biochemistry & Biophysics and serves as the Department Chair. She is also a joint Professor of Pharmacology and a preceptor for UNC IMSD, GMB, CBP, PHCO, and GI training programs. Her educational background includes a BS from the University of North Carolina at Chapel Hill, a PhD from the University of California, Berkeley, and postdoctoral training at Duke University Medical Center. Dr. Cook's research focuses on chromatin dynamics, MCM loading, and cell cycle regulation, with specific projects investigating chromatin and MCM loading dynamics, escape from G1 arrest, origin licensing control, and how cells regulate MCM loading rates. She is committed to fostering an inclusive research environment and has completed faculty mentor training, safe zone, culturally aware mentor training, REI, and mental health first aid. Her work aims to deepen understanding of cellular mechanisms governing DNA replication and cell cycle progression.

Research topics

• Biochemistry
• Biology
• Cell biology
• Genetics
• Chemistry
• Physics
• Mechanics
• Molecular biology

Selected publications

• Differential endothelial cell cycle status in postnatal retinal vessels revealed using a novel PIP-FUCCI reporter and zonation analysis

  bioRxiv (Cold Spring Harbor Laboratory) · 2024 · 1 citations

  • Cell biology
  • Biology
  • Genetics

  and reveals novel G2 regulation that may contribute to unique aspects of blood vessel network expansion.

  PublisherOA PDFDOI

• Faculty Opinions recommendation of The proliferation-quiescence decision is controlled by a bifurcation in CDK2 activity at mitotic exit.

  Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature · 2023-02-28

  dataset1st authorCorresponding
  PublisherDOI

• Faculty Opinions recommendation of DYRK1A protein kinase promotes quiescence and senescence through DREAM complex assembly.

  Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature · 2023-02-28

  dataset1st authorCorresponding
  PublisherDOI

• Faculty Opinions recommendation of E2F-dependent transcription determines replication capacity and S phase length.

  Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature · 2020-07-15

  dataset1st authorCorresponding
  PublisherDOI

• MCM Chromatin flow cytometry for cell cycle v1

  2020 · 2 citations

  Senior authorCorresponding
  • Cell biology
  • Chemistry
  • Biology

  Chromatin flow cytometry for MCM loading cell cycle analysis, adaptable to any antibody measurements by chromatin flow cytometry.

  PublisherOA PDFDOI

• Faculty Opinions recommendation of A new class of disordered elements controls DNA replication through initiator self-assembly.

  Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature · 2019-10-23

  dataset1st authorCorresponding
  PublisherDOI

• Faculty Opinions recommendation of Patterns of Early p21 Dynamics Determine Proliferation-Senescence Cell Fate after Chemotherapy.

  Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature · 2019-06-24

  dataset1st authorCorresponding
  PublisherDOI

• Replication origin licensing deficiency and genome instability during cell cycle re‐entry from quiescence

  The FASEB Journal · 2019-04-01

  article1st authorCorresponding

  Metazoan cells transition between active cell division cycles and periods of quiescence during development, regeneration, and homeostasis. Prior to cell division, DNA replication initiates during S phase at thousands of origins to ensure timely and complete genome duplication. Each origin that initiates must have been already licensed for replication in the preceding G1 phase by the DNA loading of Minichromosome Maintenance (MCM) complexes. Insufficient origin licensing in G1 causes incomplete replication and is associated with hypersensitivity to replication stress and DNA damage. We hypothesize that physiological differences in G1 length or G1 starting point impact origin licensing dynamics, and that such differences affect genome stability. We have explored origin licensing parameters in the first G1 phase during cell cycle re‐entry from quiescence relative to the G1 phases following mitosis in actively proliferating cells. We used single cell flow cytometry and live cell imaging to define the relationships among cell cycle re‐entry, G1 length, origin licensing dynamics and replication stress in untransformed human epithelial cells. Despite spending a long time in G1 phase, cells re‐entering the cell cycle are significantly under licensed in the first cell cycle but not the second or subsequent cell cycles. Cells enter their first S phase before licensing is complete and are then hypersensitive to replication stress. Thus, G1 phase upon cell cycle re‐entry is characterized by slow (or delayed) origin licensing and an apparently weak licensing checkpoint. Strikingly, repeated transitions into and out of quiescence and active proliferation exacerbate replication stress and cause hypersensitivity to replication inhibitors Therefore, the transition from quiescence to active division is a particularly sensitive time for genome stability, and the number of transitions into and out of quiescence may play a role in long term cell viability and genome stability. Support or Funding Information The UNC Flow Cytometry Core Facility is supported in part by P30 CA016086. This work was supported by a fellowship from the NSF (DGE‐1144081) to J.P.M and by grants from the NIH to J.G.C. (GM083024 and GM102413). This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .

  PublisherDOI

• Faculty Opinions recommendation of Robust Replication Control Is Generated by Temporal Gaps between Licensing and Firing Phases and Depends on Degradation of Firing Factor Sld2.

  Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature · 2019-03-31

  dataset1st authorCorresponding
  PublisherDOI

• Faculty Opinions recommendation of Lgr5+ intestinal stem cells reside in an unlicensed G1 phase.

  Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature · 2018-08-16

  dataset1st authorCorresponding

  During late mitosis and the early G 1 phase, the origins of replication are licensed by binding to double hexamers of MCM2-7.In this study, we investigated how licensing and proliferative commitment are coupled in the epithelium of the small intestine.We developed a method for identifying cells in intact tissue containing DNA-bound MCM2-7.Interphase cells above the transit-amplifying compartment had no DNA-bound MCM2-7, but still expressed the MCM2-7 protein, suggesting that licensing is inhibited immediately upon differentiation.Strikingly, we found most proliferative Lgr5 + stem cells are in an unlicensed state.This suggests that the elongated cell-cycle of intestinal stem cells is caused by an increased G 1 length, characterized by dormant periods with unlicensed origins.Significantly, the unlicensed state is lost in Apc-mutant epithelium, which lacks a functional restriction point, causing licensing immediately upon G 1 entry.We propose that the unlicensed G 1 phase of intestinal stem cells creates a temporal window when proliferative fate decisions can be made.

  PublisherDOI

Frequent coauthors

• Christopher Connolly

  14 shared

• Yabing Chen Quan

  14 shared

• Erhard Bieberich

  University of Kentucky

  14 shared

• Eefjan Breukink

  Utrecht University

  14 shared

• Julie Bouckaert

  Unité de Glycobiologie Structurale et Fonctionnelle

  14 shared

• Peter Cresswell

  Yale University

  14 shared

• Johannes Büchner

  Technical University of Munich

  14 shared

• Anita H. Corbett

  Emory University

  14 shared

Labs

• Jean Cook LabPI

Awards & honors

• American Association for the Advancement of Science (AAAS),…
• W. M. Keck Foundation Award, 2015
• Academy of Educators Elected Fellow, 2012
• The Jefferson-Pilot Fellowship in Academic Medicine, 2010-20…
• Academy of Educators Teaching Excellence Award, 2010