Journal
CHROMOSOME RESEARCH
Volume 22, Issue 3, Pages 293-303Publisher
SPRINGER
DOI: 10.1007/s10577-014-9404-1
Keywords
Centromere; Kinetochore; CENP-O; complex proteins
Funding
- Ministry of Education, Culture, Sports, Science, and Technology (MEXT) of Japan
- Precursory Research for Embryonic Science and Technology of the Japan Science and Technology Agency
- MEXT
- Grants-in-Aid for Scientific Research [26440190, 25116002, 25287099, 23310133, 21115005] Funding Source: KAKEN
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CENP-U (CENP-50) is a component of the CENP-O complex, which includes CENP-O, CENP-P, CENP-Q, CENP-R, and CENP-U and is constitutively localized at kinetochores throughout the cell cycle in vertebrates. Although CENP-U deficiency results in some mitotic defects in chicken DT40 cells, CENP-U-deficient chicken DT40 cells are viable. To examine the functional roles of CENP-U in an organism-dependent context, we generated CENP-U-deficient mice. The CENP-U-deficient mice died during early embryogenesis (approximately E7.5). Thus, conditional CENP-U-deficient mouse ES cells were generated to analyze CENP-U-deficient phenotypes at the cell level. When CENP-U was disrupted in the mouse ES cells, all CENP-O complex proteins disappeared from kinetochores. In contrast, other kinetochore proteins were recruited in CENP-U-deficient mouse ES cells as CENP-U-deficient DT40 cells. However, the CENP-U-deficient ES cells died after exhibiting abnormal mitotic behavior. Although CENP-U was essential for cell viability during mouse early embryogenesis, CENP-U-deficient mouse embryonic fibroblast cells were viable, similar to the DT40 cells. Thus, although both DT40 and ES cells with CENP-U deficiency have similar mitotic defects, cellular responses to mitotic defects vary among different cell types.
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