| Popis: |
Postembryonic neuroblasts (pNBs) in the Drosophila larval CNS are considered to be neural stem cells production most of the neurons of the adult Drosophila central nervous system (CNS). The pNBs are derived from the embryonic neuroblasts (NBs). After a period of quiescence at the end of embryogenesis they reactivate during larval life and proliferate extensively for a limited period. The pNBs are able to self-review in each division and also to produce a precursor cell that will generate two postmitotic cells that fully differentiate at metamorphosis. Therefore, the pNBs provide a good model to investigate the mechanisms involved in the regulation of neural stem cells. The aim of this research was to investigate whether Notch signalling and the transcription factor Grainyhead have roles in regulating pNBs processes. Before investigating the regulation of the pNBs behaviour it was first necessary to characterise in more detail the characteristics of these cells and their progeny. Several genes that are expressed in the embryonic CNS were selected to further study. Among these I identified some factors that are expressed only in specific pNB lineages, such as Gsb-p and others that are expressed at a specific stage in all lineages such as Prospero. Based on their expression pattern it appears that Gsb-p is likely to perform a similar function in the larval CNS as in the embryo. In contrast the distribution of Prospero suggest different roles in the pNB lineages. The result was first that the Notch pathway is active in the pNBs, indicated by the expression of Notch target gene mg. However, the results obtained, using clonal analysis to manipulate Notch function in the pNB lineages, indicate that Notch does not have a role in maintaining the undifferentiated state of the pNBs or their proliferative state. In contrast to its function in vertebrate systems where it is able to regulate the uncommitted state of the neural progenitor cells. The analysis of grh mutant indicated that Grh has a role in regulating the proliferation and/or cell death of the pNBs. |
