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dc.contributor.advisorDearden, Peter K.
dc.contributor.advisorDuncan, Elizabeth J.
dc.contributor.authorLovegrove, Mackenzie R.
dc.date.available2013-11-21T23:24:01Z
dc.date.copyright2013
dc.identifier.citationLovegrove, M. R. (2013). Genome Architecture and Phenotypic Plasticity: Is the Lethal (2) Essential for Life cluster epigenetically regulated during ovary activation in the honeybee, Apis mellifera? (Thesis, Bachelor of Biomedical Sciences with Honours). University of Otago. Retrieved from http://hdl.handle.net/10523/4489en
dc.identifier.urihttp://hdl.handle.net/10523/4489
dc.description.abstractPhenotypic plasticity is the ability of an organism to alter its phenotype, without altering its genome, in response to environmental cues. There is mounting evidence it is involved in human development, where it has been implicated in the risk of developing noncommunicable adult diseases. Studying the molecular basis of this in mammals can be difficult, particularly separating out single influences from complex environmental interactions. The honey bee, Apis mellifera, provides a useful model in which to study plasticity because of its well-controlled, easily triggered plastic responses. Queen bees are normally the only reproductively active females within a hive, but workers can activate their ovaries in response to the loss of the queen. During this process, over a third of the genome shows altered gene expression, implying that coordinated gene regulation within a chromatin domain may play a role. We have identified a candidate cluster for investigating this hypothesis, the Lethal (2) Essential for Life (L(2)efl) group. The genes of which are down-regulated as the workers undergo ovary activation. The findings of this study show that the original boundaries of the chromatin domain had been underestimated, and that the CTCF insulator element binding sites which flank the genes of the Lethal(2)efl cluster, LOC100576174 and Gmap, appear to be the boundaries of the coordinated regulation. All of the genes within these sites show co-ordinated regulation, with expression occurring in the terminal filament cells of the ovary in queens, workers and active workers. As ovary activation is a phenotypically plastic response to an environmental cue, it was hypothesised that the mechanisms which underlie it are epigenetic in nature, with previous work identifying the repressive histone mark H3K27me3 as likely playing a role in ovary activation. Potential binding sites for the ecdysteroid-regulated transcription factors BR-C Z1 and Z4 were found for all of the genes within the CTCF binding sites, and none directly outside it (LOC411452 and LOC412824). The proposed model for the coordinated regulation of the genes within the chromatin domain containing the L(2)efl group is through an interaction of both histone modifications and ecdysteroid-regulated transcription factors. This work provides evidence for large scale, coordinated changes in gene expression leading to phenotypic plasticity in response to an environmental influence.
dc.format.mimetypeapplication/pdf
dc.language.isoen
dc.publisherUniversity of Otago
dc.rightsAll items in OUR Archive are provided for private study and research purposes and are protected by copyright with all rights reserved unless otherwise indicated.
dc.subjectPhenotypic plasticity
dc.subjectApis mellifera
dc.subjectHoneybee
dc.subjectOvary Activation
dc.subjectCoordinated regulation
dc.subjectEnvironmental influence
dc.subjectLethal (2) Essential for Life
dc.titleGenome Architecture and Phenotypic Plasticity: Is the Lethal (2) Essential for Life cluster epigenetically regulated during ovary activation in the honeybee, Apis mellifera?
dc.typeThesis
dc.date.updated2013-11-21T22:50:49Z
dc.language.rfc3066en
thesis.degree.disciplineBiochemistry
thesis.degree.nameBachelor of Biomedical Sciences with Honours
thesis.degree.grantorUniversity of Otago
thesis.degree.levelHonours
otago.openaccessOpen
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