Investigating the role of DDX5/p68 RNA helicase in adipogenesis
Adipocytes are now recognized to be an essential regulator of whole-body homeostasis. The selective loss of adipose tissue results in a heterogeneous acquired or inherited disorder called lipodystrophy. Mutations in the Lamin A (LMNA) gene are known to cause Dunnigan-type familial partial lipodystro...
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| Format: | Final Year Project |
| Language: | English |
| Published: |
2014
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| Online Access: | http://hdl.handle.net/10356/61591 |
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| Institution: | Nanyang Technological University |
| Language: | English |
| Summary: | Adipocytes are now recognized to be an essential regulator of whole-body homeostasis. The selective loss of adipose tissue results in a heterogeneous acquired or inherited disorder called lipodystrophy. Mutations in the Lamin A (LMNA) gene are known to cause Dunnigan-type familial partial lipodystrophy (FPLD). Dead Box Protein 5 (DDX5)/p68 is a RNA helicase protein previously described as being important in early stages of adipogenesis. Here, the role of DDX5 in adipogenesis is characterised in more detail and its potential role as an interactor with LMNA is also examined. The protein expression of DDX5 in two different pre-adipocyte cell lines, 3T3-L1 and C3H10T/12, were highest on day two of adipogenic differentiation. The knockdown of DDX5 in differentiated 3T3-L1 cells impair adipogenesis in the early stages and results in significant decreased triglycerides accumulation. The mRNA expression of key adipogenic factor PPARγ and several other adipogenic factors were also reduced. Immunofluorescence and immunoprecipitation data suggest that DDX5 co-localizes with the lamina in 3T3-L1 cells and binds to lipodystrophic mutants of Lamin A. These results are consistent with DDX5 being crucial for adipogenesis, particularly in the early stages. Taken together, these results provide insights into the potential molecular mechanisms that underlie lipodystrophy caused by mutations in LMNA. |
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