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
-
- Spindle Apparatus/genetics
- Spindle Apparatus/pathology
- Neurogenesis/genetics
- Cell Transformation, Neoplastic/metabolism
- Apoptosis/genetics
- Nuclear Proteins/genetics
- Nuclear Proteins/metabolism*
- Chromosome Aberrations/embryology
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- RNA Interference
- Amino Acid Sequence
- RNA, Small Interfering
- Kinetochores/metabolism
- Sequence Alignment
- Gene Expression Regulation, Developmental*
- Central Nervous System/embryology*
- Central Nervous System/metabolism*
- Neurodegenerative Diseases/genetics
- Chromosomes/genetics
- Mitosis/physiology*
- Morpholinos/genetics
- Zebrafish/embryology*
- Zebrafish/genetics
- Zebrafish/metabolism*
- Animals
- 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.