Please use this identifier to cite or link to this item: http://hdl.handle.net/1783.1/7527

Defining the role of ncbp-1 and ncbp-2 to regulate sensory ray identity in C. elegans

Authors Wong, Julie Hiu Tung
Issue Date 2012
Summary Gene modulations in eukaryotes are very important for guiding the differentiation of cell types that are specialized to serve a particular function. Pre-messenger ribonucleic acid (mRNA)-splicing and microRNA processing, coupled with non-sense mediated decay are common strategies adopted to control gene expression. Cap-binding complexes, which have subunits ncbp-1 and ncbp-2, are implicated to be required in all of these events in plants to humans, which suggest that they play a conserved role in the determination of cell fate. Indeed, ncbp-1 and ncbp-2 have been found to determine the fate and identities of ray cells in Caenorhabditis elegans. I have demonstrated that by reducing the levels of either ncbp-1 or ncbp-2, this transforms the identity of ray 6 to that of ray 4, which results in rays 6-4 fusion. It has been confirmed that NCBP-1 and NCBP-2 co-localize at ray precursor cells and able to physically interact with each other via translational reporters and yeast-2-hybrid assays respectively. Therefore, it is suggested that they work together for ray patterning. In addition, ncbp-1/ncbp-2 is demonstrated to regulate ray identities by repressing Dbl/Sma signaling, rather than having a direct influence on the components of the pathway. ncbp-1/ncbp-2 is suggested to influence at the mRNA level, as it binds to the mRNA of dbl-1. This interaction is likely to be at the rays, and not at the ventral nerve cord. The findings of this study confirm the roles of ncbp-1 and ncbp-2 in cell fate determination, and inspire us on their possible mechanisms and targets.
Note Thesis (M.Phil.)--Hong Kong University of Science and Technology, 2012
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Language English
Format Thesis
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