|dc.description.abstract||The ability of an organism to change its phenotype in response to environmental change is a phenomenon termed phenotypic plasticity. Phenotypic plasticity has evolved because it allows the organism to enhance its fitness by varying its phenotype, becoming better adapted to its environment. Phenotypic plasticity may also have maladaptive consequences. If an organism changes its developmental trajectory to suit a particular environment and is exposed to a different environment, a mismatch between phenotype and environment occurs. Mismatches between phenotype and environment in humans are thought to be associated with the development of diseases such as type II diabetes and obesity. Hence it is important to understand the mechanisms underlying phenotypic plasticity.
Honeybees display remarkable examples of phenotypic plasticity. In the presence of the queen, queen mandibular pheromone (QMP) causes worker bee ovaries to be maintained in a stable inactive state. Removal of the queen, and thus QMP, causes a shift in the physiological state of the worker ovary, with changes in gene expression resulting in the activation of the worker bee ovary. The honeybee worker ovary is used as a model of phenotypic plasticity in order to determine the role epigenetic mechanisms play in establishing or maintaining phenotypic plasticity.
Genome-wide gene-expression analyses have identified genes that are differentially expressed between queen and worker ovary. Gene ontology analysis of the differentially expressed genes from the microarray analysis indicated that a significant subset of genes have roles in chromatin remodeling. Q-RT-PCR showed that the expression of the these chromatin remodeling genes changes dynamically during the process of ovary activation. Global levels of different histone modifications created by these chromatin remodeling complexes (H3K27me3 and H3K4me3) have been analysed between worker, active worker and queen ovary and have shown that histone modifications are changing in global levels during the process of ovary activation.
Chromatin immunoprecipitation, in conjunction with high throughput sequencing, allowed for genome-wide analysis of histone modifications in the honeybee ovary. This revealed that large scale gene expression changes required for the physiological remodeling of the worker ovary are in part a result of extensive genome wide changes in the enrichment of H3K27me3. Moreover the application of key inhibitors of H3K27me3 showed that H3K27me3 inhibition significantly increases activation of the ovary and therefore implicates H3K27me3 as playing a key role in honeybee ovary activation. This research will have implications not only for understanding how phenotypic plasticity is established in honeybee but will contribute to a wider knowledge of the role phenotypic plasticity plays in evolution and development, and human health and disease.||