Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Cycloheximide-induced mitotic delay in Physarum polycephalum.

C Scheffey1, J J Wille

  • 1Department of Biophysics and Theoretical Biology, University of Chicago, IL 60637.

Experimental Cell Research
|May 1, 1978
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Ionic currents flow through Micrasterias and Closterium cells during expansion of the primary cell wall.

Planta·2013
Same author

Palmitoleic acid isomer (C16:1delta6) in human skin sebum is effective against gram-positive bacteria.

Skin pharmacology and applied skin physiology·2003
Same author

Inhibition of irritation and contact hypersensitivity by phenoxyacetic acid methyl ester in mice.

Skin pharmacology and applied skin physiology·2000
Same author

Several different ion channel modulators abrogate contact hypersensitivity in mice.

Skin pharmacology and applied skin physiology·1999
Same author

cis-urocanic acid induces mast cell degranulation and release of preformed TNF-alpha: A possible mechanism linking UVB and cis-urocanic acid to immunosuppression of contact hypersensitivity.

Skin pharmacology and applied skin physiology·1999
Same author

Inhibition of irritation and contact hypersensitivity by ethacrynic acid.

Skin pharmacology and applied skin physiology·1999

Cycloheximide pulses applied to Physarum polycephalum delay mitosis, with the delay duration depending on when the pulse occurs during the cell cycle. The study quantizes this relationship for G2 phase exposure.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Understanding cell cycle regulation is crucial for cell biology.
  • Physarum polycephalum is a model organism for studying nuclear division and cell cycle dynamics.
  • Cycloheximide is a known inhibitor of protein synthesis, impacting cellular processes.

Purpose of the Study:

  • To investigate the effect of cycloheximide pulses on mitosis in Physarum polycephalum.
  • To determine the relationship between the timing of cycloheximide application in the cell cycle and the resulting mitotic delay.
  • To quantify the dose- and time-dependent delay of mitosis induced by cycloheximide.

Main Methods:

  • Application of controlled cycloheximide pulses to Physarum polycephalum surface plasmodia.

Related Experiment Videos

  • Precise timing of pulse initiation relative to mitosis.
  • Measurement of mitotic delay and calculation of excess delay.
  • Analysis of the linear dependence of mitotic delay on cell cycle phase.

    • Main Results:

    • Cycloheximide pulses applied during the G2 phase of the cell cycle induce a delay in mitosis.
    • The delay is linearly dependent on the specific phase within G2 when the pulse is applied.
    • A formula was derived: excess delay = (0.55)t - 1.3 hours for a 30-minute pulse starting at time 't' after mitosis.
    • Longer pulses (7 hours) showed a maximum excess delay of approximately 1 hour.
    • Pulses applied shortly before mitosis (within 30 minutes) resulted in minimal delays.

    Conclusions:

    • Cycloheximide effectively delays mitosis in Physarum polycephalum in a cell cycle-dependent manner.
    • The quantitative relationship established provides insight into cell cycle checkpoints and protein synthesis requirements.
    • These findings contribute to understanding the temporal regulation of mitosis and the impact of protein synthesis inhibition.