Abstract
BackgroundWe 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.ResultsTo 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.ConclusionsTherefore, 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.
Highlights
We recently identified a novel oncogene, Cancer-upregulated gene 2 (CUG2), which is essential for kinetochore formation and promotes tumorigenesis in mammalian cells
CUG2 was shown to interact with CENP-T and CENP-A, essential components of the nucleosome complex located at the centromere, and was named centromere protein W (CENP-W) [2,3]
Our results indicate that Cug2 is essential for normal mitosis and central nervous system (CNS) development, and that loss of Cug2 function lead to neurodegenerative phenotypes
Summary
We recently identified a novel oncogene, Cancer-upregulated gene 2 (CUG2), which is essential for kinetochore formation and promotes tumorigenesis in mammalian cells. The in vivo function of CUG2 has not been studied in animal models. Cancer-upregulated gene 2 (CUG2) is known to be differentially expressed in multiple human cancer tissues including the ovary, liver, lung, intestines and pancreas [1]. CUG2 was shown to interact with CENP-T and CENP-A, essential components of the nucleosome complex located at the centromere, and was named centromere protein W (CENP-W) [2,3]. To elucidate the endogenous function of CUG2 in vivo, we investigated the expression patterns and potential roles of cug in zebrafish during early embryogenesis. Our results indicate that Cug is essential for normal mitosis and CNS development, and that loss of Cug function lead to neurodegenerative phenotypes
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