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dc.identifier.urihttp://hdl.handle.net/11401/76172
dc.description.sponsorshipThis work is sponsored by the Stony Brook University Graduate School in compliance with the requirements for completion of degree.en_US
dc.formatMonograph
dc.format.mediumElectronic Resourceen_US
dc.language.isoen_US
dc.publisherThe Graduate School, Stony Brook University: Stony Brook, NY.
dc.typeDissertation
dcterms.abstractCanalization is the ability of an organism's phenotype to remain stable under a perturbation in their genotype or the environment. It has been noted that there is no canalization or canalization is to a much smaller degree in mutants than in wild type. Waddington's idea was to understand canalization through studying gene interactions. We investigate the mechanisms of canalization of gap gene patterns in </italic>D.melanogaster</italic> through dynamical analysis of the gene circuit. To carry out this investigation we construct a dynamical model of the evolution of the concentration of protein products of the gap genes in time. Our model, which is fitted to both wild type and </italic>Kr<super>-<super></italic> data, correctly captures the wild type averaged data and the lowered gap gene expression in </italic>Kr<super>-<super></italic>. Through a dynamical analysis on a simplified version of this model, we investigate pattern formation in both wild type and </italic>Kr<super>-<super></italic>. The analysis is concentrated on the gap genes </italic>hb</italic>, </italic>Kr</italic>, </italic>gt</italic> and </italic>kni</italic> with outside input from maternal genes </italic>bcd</italic> and </italic>Cad</italic>. Canalization manifests itself in this model by producing a lower variance, in wild type, of posterior </italic>gt</italic> domain, in comparison to Bcd. </italic>Kr<super>-<super></italic> mutants do not canalize Bcd perturbation. We find the geometric structure that ensures the canalization in wild type. This structure is an unstable manifold that patterns the posterior of the wild type embryos while remaining invariant with respect to changes in Bcd. By continuously changing one parameter in our model (maximum synthesis rate of </italic>Kr</italic>), we can smoothly turn down the function of </italic>Kr</italic> in such a way as to model an allelic series running from homozygous wild type levels to heterozygous, and then to hypomorphic and finally to functional null. We discovered that that there is an abrupt onset of the mutant phenotype and loss of canalization triggered by the loss of the canalizing unstable manifold.
dcterms.available2017-09-20T16:42:34Z
dcterms.contributorGreen, Daviden_US
dcterms.contributorReinitz, Johnen_US
dcterms.contributorDeng, Yuefanen_US
dcterms.contributorMartens, Marco.en_US
dcterms.creatorPanok, Lena
dcterms.dateAccepted2017-09-20T16:42:34Z
dcterms.dateSubmitted2017-09-20T16:42:34Z
dcterms.descriptionDepartment of Applied Mathematics and Statistics.en_US
dcterms.extent135 pg.en_US
dcterms.formatMonograph
dcterms.formatApplication/PDFen_US
dcterms.identifierhttp://hdl.handle.net/11401/76172
dcterms.issued2013-12-01
dcterms.languageen_US
dcterms.provenanceMade available in DSpace on 2017-09-20T16:42:34Z (GMT). No. of bitstreams: 1 Panok_grad.sunysb_0771E_11512.pdf: 9310488 bytes, checksum: 338ed028120d4286b532d22c96407c85 (MD5) Previous issue date: 1en
dcterms.publisherThe Graduate School, Stony Brook University: Stony Brook, NY.
dcterms.subjectcanalization, dynamical analysis, pattern formation
dcterms.subjectApplied mathematics
dcterms.titleThe Dynamical Basis of the Decanalization of Gene Expression in Kr uppel Mutant Embryos
dcterms.typeDissertation


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