Translational Control and the Cell Cycle

2004 ◽  
pp. 397-448 ◽  
Author(s):  
Robert E. Rhoads
2021 ◽  
Vol 22 (11) ◽  
pp. 5483
Author(s):  
Luisa F. Bustamante-Jaramillo ◽  
Celia Ramos ◽  
Cristina Martín-Castellanos

Cyclins and CDKs (Cyclin Dependent Kinases) are key players in the biology of eukaryotic cells, representing hubs for the orchestration of physiological conditions with cell cycle progression. Furthermore, as in the case of meiosis, cyclins and CDKs have acquired novel functions unrelated to this primal role in driving the division cycle. Meiosis is a specialized developmental program that ensures proper propagation of the genetic information to the next generation by the production of gametes with accurate chromosome content, and meiosis-specific cyclins are widespread in evolution. We have explored the diversification of CDK functions studying the meiosis-specific Crs1 cyclin in fission yeast. In addition to the reported role in DSB (Double Strand Break) formation, this cyclin is required for meiotic S-phase progression, a canonical role, and to maintain the architecture of the meiotic chromosomes. Crs1 localizes at the SPB (Spindle Pole Body) and is required to stabilize the cluster of telomeres at this location (bouquet configuration), as well as for normal SPB motion. In addition, Crs1 exhibits CDK(Cdc2)-dependent kinase activity in a biphasic manner during meiosis, in contrast to a single wave of protein expression, suggesting a post-translational control of its activity. Thus, Crs1 displays multiple functions, acting both in cell cycle progression and in several key meiosis-specific events.


2001 ◽  
Vol 11 (1) ◽  
pp. 13-18 ◽  
Author(s):  
Stéphane Pyronnet ◽  
Nahum Sonenberg

2017 ◽  
Vol 36 (4) ◽  
pp. 487-502 ◽  
Author(s):  
Heidi M Blank ◽  
Ricardo Perez ◽  
Chong He ◽  
Nairita Maitra ◽  
Richard Metz ◽  
...  

Cell ◽  
2002 ◽  
Vol 109 (4) ◽  
pp. 473-483 ◽  
Author(s):  
Irina Groisman ◽  
Mi-Young Jung ◽  
Madathia Sarkissian ◽  
Quiping Cao ◽  
Joel D Richter

2010 ◽  
Vol 12 (5) ◽  
pp. 447-456 ◽  
Author(s):  
Isabel Novoa ◽  
Javier Gallego ◽  
Pedro G. Ferreira ◽  
Raul Mendez

2009 ◽  
Vol 29 (10) ◽  
pp. 2841-2851 ◽  
Author(s):  
Rafael Cuesta ◽  
Aida Martínez-Sánchez ◽  
Fátima Gebauer

ABSTRACT p27kip1 (p27) is a cell cycle inhibitor and tumor suppressor whose expression is tightly regulated in the cell. Translational control of p27 mRNA has emerged as a prominent mechanism to regulate p27 expression during differentiation, quiescence, and cancer progression. The microRNAs miR-221 and miR-222 repress p27 expression in various cancer cells, and this repression promotes tumor cell proliferation. In addition, the presence of an internal ribosome entry site in the 5′ untranslated region (UTR) of p27 mRNA has been reported. Here, we show that p27 mRNA is translated via a cap-dependent mechanism in HeLa and HL60 cells and that the previously reported IRES activity can be attributed to cryptic promoters in the sequence corresponding to the p27 5′ UTR. Furthermore, cap-dependent translation of p27 mRNA is repressed by miR-181a in undifferentiated HL60 cells. Repression by miR-181a is relieved during differentiation of HL60 into monocyte-like cells, allowing the accumulation of p27, which is necessary to fully block cell cycle progression and reach terminal differentiation. These results identify miR-181a as a regulator of p27 mRNA translation during myeloid cell differentiation.


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