Project description:This a model from the article:
Limit cycle models for circadian rhythms based on transcriptional regulation in Drosophila and Neurospora.
Leloup JC, Gonze D, Goldbeter A.
J Biol Rhythms.1999 Dec;14(6):433-48.
10643740,
Abstract:
We examine theoretical models for circadian oscillations based on transcriptional regulation in Drosophila and Neurospora. For Drosophila, the molecular model is based on the negative feedback exerted on the expression of the per and tim genes by the complex formed between the PER and TIM proteins. For Neurospora, similarly, the model relies on the feedback exerted on the expression of the frq gene by its protein product FRQ. In both models, sustained rhythmic variations in protein and mRNA levels occur in continuous darkness, in the form of limit cycle oscillations. The effect of light on circadian rhythms is taken into account in the models by considering that it triggers degradation of the TIM protein in Drosophila, and frq transcription in Neurospora. When incorporating the control exerted by light at the molecular level, we show that the models can account for the entrainment of circadian rhythms by light-dark cycles and for the damping of the oscillations in constant light, though such damping occurs more readily in the Drosophila model. The models account for the phase shifts induced by light pulses and allow the construction of phase response curves. These compare well with experimental results obtained in Drosophila. The model for Drosophila shows that when applied at the appropriate phase, light pulses of appropriate duration and magnitude can permanently or transiently suppress circadian rhythmicity. We investigate the effects of the magnitude of light-induced changes on oscillatory behavior. Finally, we discuss the common and distinctive features of circadian oscillations in the two organisms.
This particular version of the model has been translated from equations 1a-1j (Drosophila).
This model was taken from the
CellML repository and automatically converted to SBML.
The original model was:
Leloup JC, Gonze D, Goldbeter A. (1999) - version02
The original CellML model was created by:
Lloyd, Catherine, May
c.lloyd@aukland.ac.nz
The University of Auckland
The Bioengineering Institute
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
For more information see the terms of use.
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
Project description:This a model from the article:
Limit cycle models for circadian rhythms based on transcriptional regulation in Drosophila and Neurospora.
Leloup JC, Gonze D, Goldbeter A. J Biol Rhythms.
1999 Dec;14(6):433-48. 10643740
,
Abstract:
We examine theoretical models for circadian oscillations based on transcriptional regulation in Drosophila and Neurospora. For Drosophila, the molecular model is based on the negative feedback exerted on the expression of the per and tim genes by the complex formed between the PER and TIM proteins. For Neurospora, similarly, the model relies on the feedback exerted on the expression of the frq gene by its protein product FRQ. In both models, sustained rhythmic variations in protein and mRNA levels occur in continuous darkness, in the form of limit cycle oscillations. The effect of light on circadian rhythms is taken into account in the models by considering that it triggers degradation of the TIM protein in Drosophila, and frq transcription in Neurospora. When incorporating the control exerted by light at the molecular level, we show that the models can account for the entrainment of circadian rhythms by light-dark cycles and for the damping of the oscillations in constant light, though such damping occurs more readily in the Drosophila model. The models account for the phase shifts induced by light pulses and allow the construction of phase response curves. These compare well with experimental results obtained in Drosophila. The model for Drosophila shows that when applied at the appropriate phase, light pulses of appropriate duration and magnitude can permanently or transiently suppress circadian rhythmicity. We investigate the effects of the magnitude of light-induced changes on oscillatory behavior. Finally, we discuss the common and distinctive features of circadian oscillations in the two organisms.
This particular version of the model has been translated from equations 4a-4c (Neurospora).
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was: Leloup JC, Gonze D, Goldbeter A. (1999) - version02
The original CellML model was created by:
Lloyd, Catherine, May
c.lloyd@aukland.ac.nz
The University of Auckland
The Bioengineering Institute
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2010 The BioModels.net Team.
For more information see the terms of use
.
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
Project description:By performing RNA-seq analysis on ALKBH5-deficient (ALKBH5-/-, KO) and Wild-type (WT) dHL-60 human neutrophils infected with Escherichia coli, we want to investigate the effect of ALKBH5 on transcriptional landscape of human neutrophils during bacterial infection. Then, we performed gene expression profiling and Gene Ontology enrichment analysis of the significantly differentially expressed genes using data obtained from RNA-seq.
Project description:By performing RNA-seq analysis on bone marrow neutrophils from the Alkbh5-deficient mice and Wild-type littermates undergoing CLP-induced sepsis, we want to investigate the effect of ALKBH5 on transcriptional landscape of mouse bone marrow neutrophils during bacterial infection. Then, we performed gene expression profiling and Gene Ontology enrichment analysis of the significantly differentially expressed genes using data obtained from RNA-seq.
Project description:We investigate the biological effects of radiation using Drosophila Melanogaster as a model organism, focusing on gene expression and lifespan analysis to determine the effect of different radiation doses. Our results support a threshold effect in response to radiation: no effect on lifespan and no permanent effect on gene expression is seen at doses below 10,000 Roentgens. Adult male Drosophila were irradiated 2 days after eclosion, with one of 6 radiation doses: 10; 1,000; 5,000; 10,000; 20,000 Roentgens. Samples were taken at 3 time points (2, 10 and 20 days post-irradiation).
Project description:To investigate the effect of sex on within- and between-population variation in gene expression, we performed a microarray analysis of adult females from 16 strains of Drosophila melanogaster, including eight strains from the putative ancestral range in sub-Saharan Africa and eight strains from a European population. The results were compared to those of a previous study of adult male gene expression variation among the same strains (GSE8843).
Project description:The effect of germline tissue on somatic sex-biased expression is examined. Expression is assayed in various adult tissues with germline ablated directly or genetically. The effect of germline signalling on sex-biased expression in the Drosophila head is also examined. Keywords: Expression profiling
Project description:To investigate transcriptional effects caused by a severe defect in endo-siRNA production, a gene expression profiling was performed on Drosophila dicer-2 pupae compared to wild-type.
Project description:Transcriptional profiling of mouse macrophage cells comparing control untreated cells with macrophage cells infected with Burkeholderia pseudomallei. Goal was to determine the effects of bacterial infection on global macrophage gene expression.