Format

Send to

Choose Destination
See comment in PubMed Commons below
Cell Cycle. 2016 Jul 17;15(14):1855-64. doi: 10.1080/15384101.2016.1188238. Epub 2016 May 18.

Cyc17, a meiosis-specific cyclin, is essential for anaphase initiation and chromosome segregation in Tetrahymena thermophila.

Author information

1
a Key Laboratory of Aquatic Biodiversity and Conservation, Institute of Hydrobiology, Chinese Academy of Sciences , Wuhan , People's Republic of China.
2
b University of Chinese Academy of Sciences , Beijing , People's Republic of China.
3
c College of Life Sciences, Northwest Normal University , Lanzhou , People's Republic of China.
4
d Department of Chromosome Biology and Max F. Perutz Laboratories , Center for Molecular Biology, University of Vienna , Vienna , Austria.

Abstract

Although the role of cyclins in controlling nuclear division is well established, their function in ciliate meiosis remains unknown. In ciliates, the cyclin family has undergone massive expansion which suggests that diverse cell cycle systems exist, and this warrants further investigation. A screen for cyclins in the model ciliate Tetrahymena thermophila showed that there are 34 cyclins in this organism. Only 1 cyclin, Cyc17, contains the complete cyclin core and is specifically expressed during meiosis. Deletion of CYC17 led to meiotic arrest at the diakinesis-like metaphase I stage. Expression of genes involved in DNA metabolism and chromosome organization (chromatin remodeling and basic chromosomal structure) was repressed in cyc17 knockout matings. Further investigation suggested that Cyc17 is involved in regulating spindle pole attachment, and is thus essential for chromosome segregation at meiosis. These findings suggest a simple model in which chromosome segregation is influenced by Cyc17.

KEYWORDS:

Tetrahymena thermophila; anaphase initiation; chromosome segregation; cyclin; meiosis

PMID:
27192402
PMCID:
PMC4968904
DOI:
10.1080/15384101.2016.1188238
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Taylor & Francis Icon for PubMed Central
    Loading ...
    Support Center