Licensing Factor

2020 ◽  
Author(s):  
Keyword(s):  
Licensing Factor

A murine replication protein accumulates temporarily in the heterochromatic regions of nuclei prior to initiation of DNA replication

1995 ◽  
Vol 108 (3) ◽  
pp. 927-934 ◽  
Author(s):  
M. Starborg ◽  
E. Brundell ◽  
K. Gell ◽  
C. Larsson ◽  
I. White ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Replication ◽  
Mammalian Cells ◽  
Mitotic Cell ◽  
Yeast Cells ◽  
Metaphase Chromosomes ◽  
Licensing Factor ◽  
Mammalian Homologue ◽  
Initiation Of Dna Replication

We have analyzed the expression of the murine P1 gene, the mammalian homologue of the yeast MCM3 protein, during the mitotic cell cycle. The MCM3 protein has previously been shown to be of importance for initiation of DNA replication in Saccharomyces cerevisiae. We found that the murine P1 protein was present in the nuclei of mammalian cells throughout interphase of the cell cycle. This is in contrast to the MCM3 protein, which is located in the nuclei of yeast cells only between the M and the S phase of the cell cycle. Detailed analysis of the intranuclear localization of the P1 protein during the cell cycle revealed that it accumulates transiently in the heterochromatic regions towards the end of G1. The accumulation of the P1 protein in the heterochromatic regions prior to activation of DNA replication suggests that the mammalian P1 protein is also of importance for initiation of DNA replication. The MCM2-3.5 proteins have been suggested to represent yeast equivalents of a hypothetical replication licensing factor initially described in Xenopus. Our data support this model and indicate that the murine P1 protein could function as replication licensing factor. The chromosomal localization of the P1 gene was determined by fluorescence in situ hybridization to region 6p12 in human metaphase chromosomes.

DNA replication licensing factor

1996 ◽  
pp. 83-90 ◽  
Author(s):  
James P. J. Chong ◽  
J. Julian Blow
Keyword(s):  
Dna Replication ◽  
Licensing Factor

scholarly journals Cyclin A Promotes S-Phase Entry via Interaction with the Replication Licensing Factor Mcm7

2010 ◽  
Vol 31 (2) ◽  
pp. 248-255 ◽  
Author(s):  
T. Chibazakura ◽  
K. Kamachi ◽  
M. Ohara ◽  
S. Tane ◽  
H. Yoshikawa ◽  
...  
Keyword(s):  
Cyclin A ◽  
S Phase ◽  
Licensing Factor ◽  
Phase Entry

scholarly journals The Licensing Factor Cdt1 Links Cell Cycle Progression to the DNA Damage Response

2020 ◽  
Vol 40 (5) ◽  
pp. 2449-2456
Author(s):  
ALEXANDRA KANELLOU ◽  
NICKOLAOS NIKIFOROS GIAKOUMAKIS ◽  
ANDREAS PANAGOPOULOS ◽  
SPYRIDON CHAMPERIS TSANIRAS ◽  
ZOI LYGEROU
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Dna Damage Response ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Damage Response ◽  
Licensing Factor

scholarly journals The Caenorhabditis elegans Replication Licensing Factor CDT-1 Is Targeted for Degradation by the CUL-4/DDB-1 Complex

2006 ◽  
Vol 27 (4) ◽  
pp. 1394-1406 ◽  
Author(s):  
Youngjo Kim ◽  
Edward T. Kipreos
Keyword(s):  
Caenorhabditis Elegans ◽  
Ubiquitin Ligase ◽  
S Phase ◽  
Null Mutant ◽  
Wild Type ◽  
C Elegans ◽  
Licensing Factor ◽  
Ubiquitin Ligase E3 ◽  
Blast Cells ◽  
Temporal Restriction

ABSTRACT The replication of genomic DNA is strictly regulated to occur only once per cell cycle. This regulation centers on the temporal restriction of replication licensing factor activity. Two distinct ubiquitin ligase (E3) complexes, CUL4/DDB1 and SCFSkp2, have been reported to target the replication licensing factor Cdt1 for ubiquitin-mediated proteolysis. However, it is unclear to what extent these two distinct Cdt1 degradation pathways are conserved. Here, we show that Caenorhabditis elegans DDB-1 is required for the degradation of CDT-1 during S phase. DDB-1 interacts specifically with CUL-4 but not with other C. elegans cullins. A ddb-1 null mutant exhibits extensive DNA rereplication in postembryonic BLAST cells, similar to what is observed in cul-4(RNAi) larvae. DDB-1 physically associates with CDT-1, suggesting that CDT-1 is a direct substrate of the CUL-4/DDB-1 E3 complex. In contrast, a deletion mutant of the C. elegans Skp2 ortholog, skpt-1, appears overtly wild type with the exception of an impenetrant gonad migration defect. There is no appreciable role for SKPT-1 in the degradation of CDT-1 during S phase, even in a sensitized ddb-1 mutant background. We propose that the CUL-4/DDB-1 ubiquitin ligase is the principal E3 for regulating the extent of DNA replication in C. elegans.

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