Human Topoisomerase IIalpha is Phosphorylated in a Cell-Cycle Phase-Dependent Manner by a Proline-Directed Kinase

1995 ◽  
Vol 231 (2) ◽  
pp. 491-497 ◽  
Author(s):  
Nicholas J. Wells ◽  
Ian D. Hickson
2003 ◽  
Vol 23 (2) ◽  
pp. 708-720 ◽  
Author(s):  
Jong Heon Kim ◽  
Ki Young Paek ◽  
Kobong Choi ◽  
Tae-Don Kim ◽  
Bumsuk Hahm ◽  
...  

ABSTRACT The c-myc proto-oncogene plays a key role in the proliferation, differentiation, apoptosis, and regulation of the cell cycle. Recently, it was demonstrated that the 5′ nontranslated region (5′ NTR) of human c-myc mRNA contains an internal ribosomal entry site (IRES). In this study, we investigated cellular proteins interacting with the IRES element of c-myc mRNA. Heterogeneous nuclear ribonucleoprotein C (hnRNP C) was identified as a cellular protein that interacts specifically with a heptameric U sequence in the c-myc IRES located between two alternative translation initiation codons CUG and AUG. Moreover, the addition of hnRNP C1 in an in vitro translation system enhanced translation of c-myc mRNA. Interestingly, hnRNP C was partially relocalized from the nucleus, where most of the hnRNP C resides at interphase, to the cytoplasm at the G2/M phase of the cell cycle. Coincidently, translation mediated through the c-myc IRES was increased at the G2/M phase when cap-dependent translation was partially inhibited. On the other hand, a mutant c-myc mRNA lacking the hnRNP C-binding site, showed a decreased level of translation at the G2/M phase compared to that of the wild-type message. Taken together, these findings suggest that hnRNP C, via IRES binding, modulates translation of c-myc mRNA in a cell cycle phase-dependent manner.


PLoS ONE ◽  
2012 ◽  
Vol 7 (4) ◽  
pp. e34386 ◽  
Author(s):  
Alessandra Galati ◽  
Frédérique Magdinier ◽  
Valentina Colasanti ◽  
Serge Bauwens ◽  
Sébastien Pinte ◽  
...  

2016 ◽  
Vol 119 (3) ◽  
pp. 544-551 ◽  
Author(s):  
Yan Liu ◽  
Weiqiang Chen ◽  
Pengcheng Zhang ◽  
Xiaodong Jin ◽  
Xinguo Liu ◽  
...  

1984 ◽  
Vol 70 (1) ◽  
pp. 133-145 ◽  
Author(s):  
C.J. Weijer ◽  
G. Duschl ◽  
C.N. David

The relationship between the cell cycle phase of vegetative amoebae and prestalk and prespore differentiation in the slug stage were investigated in the slime mould Dictyostelium discoideum. Cells were synchronized by release from the stationary phase. Samples were taken at various times during the course of a synchronous cell doubling, fluorescently labelled and mixed with cells of random cell cycle phase from exponentially growing cultures. The fate of the fluorescently labelled cells was recorded at the slug stage. Cells early in the cycle exhibit strong prestalk sorting; cells taken later in the cycle exhibit strong prespore sorting. The period of prestalk sorting occurs immediately following mitosis and lasts about 1 h in a cell cycle of about 7 h duration. Accompanying the altered sorting behaviour is a marked changed in the prestalk-prespore proportions in slugs formed from synchronized populations of cells. Cells synchronized early in the cycle form slugs with 55% prespore cells; cells synchronized late in the cycle form slugs with 90% prespore. The results are discussed in terms of models for the formation of the prestalk-prespore pattern in slugs.


Open Biology ◽  
2020 ◽  
Vol 10 (5) ◽  
pp. 190259
Author(s):  
Simon Gemble ◽  
Géraldine Buhagiar-Labarchède ◽  
Rosine Onclercq-Delic ◽  
Gaëlle Fontaine ◽  
Sarah Lambert ◽  
...  

Topoisomerase IIα (Topo IIα), a well-conserved double-stranded DNA (dsDNA)-specific decatenase, processes dsDNA catenanes resulting from DNA replication during mitosis. Topo IIα defects lead to an accumulation of ultrafine anaphase bridges (UFBs), a type of chromosome non-disjunction. Topo IIα has been reported to resolve DNA anaphase threads, possibly accounting for the increase in UFB frequency upon Topo IIα inhibition. We hypothesized that the excess UFBs might also result, at least in part, from an impairment of the prevention of UFB formation by Topo IIα. We found that Topo IIα inhibition promotes UFB formation without affecting the global disappearance of UFBs during mitosis, but leads to an aberrant UFB resolution generating DNA damage within the next G1. Moreover, we demonstrated that Topo IIα inhibition promotes the formation of two types of UFBs depending on cell cycle phase. Topo IIα inhibition during S-phase compromises complete DNA replication, leading to the formation of UFB-containing unreplicated DNA, whereas Topo IIα inhibition during mitosis impedes DNA decatenation at metaphase–anaphase transition, leading to the formation of UFB-containing DNA catenanes. Thus, Topo IIα activity is essential to prevent UFB formation in a cell-cycle-dependent manner and to promote DNA damage-free resolution of UFBs.


Cells ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 2112
Author(s):  
Fatma Rabia Urun ◽  
Adrian W Moore

In neural precursors, cell cycle regulators simultaneously control both progression through the cell cycle and the probability of a cell fate switch. Precursors act in lineages, where they transition through a series of cell types, each of which has a unique molecular identity and cellular behavior. Thus, investigating links between cell cycle and cell fate control requires simultaneous identification of precursor type and cell cycle phase, as well as an ability to read out additional regulatory factor expression or activity. We use a combined FUCCI-EdU labelling protocol to do this, and then apply it to the embryonic olfactory neural lineage, in which the spatial position of a cell correlates with its precursor identity. Using this integrated model, we find the CDKi p27KIP1 has different regulation relative to cell cycle phase in neural stem cells versus intermediate precursors. In addition, Hes1, which is the principle transcriptional driver of neural stem cell self-renewal, surprisingly does not regulate p27KIP1 in this cell type. Rather, Hes1 indirectly represses p27KIP1 levels in the intermediate precursor cells downstream in the lineage. Overall, the experimental model described here enables investigation of cell cycle and cell fate control linkage from a single precursor through to a lineage systems level.


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