Please use this identifier to cite or link to this item: https://libjncir.jncasr.ac.in/xmlui/handle/10572/186
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dc.contributor.authorRuoff, Peter-
dc.contributor.authorChristensen, Melinda K-
dc.contributor.authorSharma, Vijay Kumar-
dc.date.accessioned2012-01-16T09:55:05Z-
dc.date.available2012-01-16T09:55:05Z-
dc.date.issued2005-11-07-
dc.identifier0022-5193en_US
dc.identifier.citationJournal Of Theoretical Biology 237(1), 41-57 (2005)en_US
dc.identifier.urihttps://libjncir.jncasr.ac.in/xmlui/10572/186-
dc.descriptionRestricted Accessen_US
dc.description.abstractWe have analysed a first-order kinetic representation of a interlocking-feedback loop model for the Drosophila circadian clock. In this model, the transcription factor Drosophila CLOCK (dCLK) which activates the clock genes period (per) and timeless (tim) is subjected to positive and negative regulations by the proteins 'PAR Domain Protein 1' (PDP1) and VRILLE (VRI), whose transcription is activated by dCLK. The PER/TIM complex binds to dCLK and in this way reduces the activity of dCLK. The results of our simulations suggest that the positive and negative feedback loops of Pdp1 and vri are essential for the overall oscillations. Although self sustained oscillations can be obtained without per/tim, the model shows that the PER/TIM complex plays an important role in amplification and stabilization of the oscillations generated by the Pdp1/vri positive/negative feedback loops. We further show that in contrast to a single (per/tim) negative feedback loop oscillator, the interlocking-feedback loop model can readily account for the effect of gene dosages of per, vri, and Pdp1 on the period length. Calculations of phase resetting on a temperature compensated version of the model shows good agreement with experimental phase response curves for high and low temperature pulses. Also, the partial losses of temperature compensation in per(S) and per(L) mutants can be described, which are related to decreased stabilities of the PER/TIM complex in per(S) and the stronger/more stable inhibitory complex between dCLK and PER/TIM in per(L), respectively. The model shows (somewhat surprisingly) poor entrainment properties, especially under extended light/dark (L/D) cycles, which suggests that parts of the L/D tracking or sensing system are not well represented. (c) 2005 Elsevier Ltd. All rights reserved.en_US
dc.description.urihttp://dx.doi.org//10.1016/j.jtbi.2005.03.030en_US
dc.language.isoenen_US
dc.publisherAcademic Press Ltd Elsevier Science Ltden_US
dc.rights© 2005 Elsevier Ltden_US
dc.subjectcircadian oscillationsen_US
dc.subjectDrosophilaen_US
dc.subjecttemperature compensationen_US
dc.subjectgene dosageen_US
dc.subjectinterlocking-feedback loopen_US
dc.subjectmolecular amplificationen_US
dc.subjectPDP1en_US
dc.subjectVRILLEen_US
dc.subjectPERIODen_US
dc.subjectTIMELESSen_US
dc.subjectCrassulacean Acid Metabolismen_US
dc.subjectPer-Tim Complexen_US
dc.subjectGoodwin Modelen_US
dc.subjectSporulation Rhythmen_US
dc.subjectLocomotor-Activityen_US
dc.subjectNeurospora-Crassaen_US
dc.subjectMolecular-Basesen_US
dc.subjectLight-Pulsesen_US
dc.subjectOscillatoren_US
dc.subjectProteinen_US
dc.titlePER/TIM-mediated amplification, gene dosage effects and temperature compensation in an interlocking-feedback loop model of the Drosophila circadian clocken_US
dc.typeArticleen_US
Appears in Collections:Research Articles (V. K. Sharma)

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