Cug2 is essential for normal mitotic control and CNS development in zebrafish
- Authors
- Kim, H.T., So, J.H., Jung, S.H., Ahn, D.G., Koh, W., Kim, N.S., Kim, S.H., Lee, S., and Kim, C.H.
- ID
- ZDB-PUB-110816-18
- Date
- 2011
- Source
- BMC Developmental Biology 11(1): 49 (Journal)
- Registered Authors
- Ahn, Dae-gwon, Jung, Seung-Hyun, Kim, Cheol-Hee, Kim, Hyun-Taek, So, Ju-Hoon
- Keywords
- none
- MeSH Terms
-
- Amino Acid Sequence
- Animals
- Apoptosis/genetics
- Cell Transformation, Neoplastic/metabolism
- Central Nervous System/embryology*
- Central Nervous System/metabolism*
- Chromosome Aberrations/embryology
- Chromosomes/genetics
- Gene Expression Regulation, Developmental*
- Kinetochores/metabolism
- Mitosis/physiology*
- Morpholinos/genetics
- Neurodegenerative Diseases/genetics
- Neurogenesis/genetics
- Nuclear Proteins/genetics
- Nuclear Proteins/metabolism*
- RNA Interference
- RNA, Small Interfering
- Sequence Alignment
- Spindle Apparatus/genetics
- Spindle Apparatus/pathology
- Zebrafish/embryology*
- Zebrafish/genetics
- Zebrafish/metabolism*
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- PubMed
- 21838932 Full text @ BMC Dev. Biol.
Background
We recently identified a novel oncogene, Cancer-upregulated gene 2 (CUG2), which is essential for kinetochore formation and promotes tumorigenesis in mammalian cells. However, the in vivo function of CUG2 has not been studied in animal models.
Results
To study the function of CUG2 in vivo, we isolated a zebrafish homologue that is expressed specifically in the proliferating cells of the central nervous system (CNS). Morpholino-mediated knockdown of cug2 resulted in apoptosis throughout the CNS and the development of neurodegenerative phenotypes. In addition, cug2-deficient embryos contained mitotically arrested cells displaying abnormal spindle formation and chromosome misalignment in the neural plate.
Conclusions
Therefore, our findings suggest that Cug2 is required for normal mitosis during early neurogenesis and has functions in neuronal cell maintenance, thus demonstrating that the cug2 deficient embryos may provide a model system for human neurodegenerative disorders.