Human Raf-1 proteins associate with Rad24 and Cdc25 in cell-cycle checkpoint pathway of fission yeast,Schizosaccharomyces pombe

2007 ◽  
Vol 101 (2) ◽  
pp. 488-497 ◽  
Author(s):  
Michael Lee ◽  
Hyang-Sook Yoo
Keyword(s):  
Cell Cycle ◽  
Schizosaccharomyces Pombe ◽  
Fission Yeast ◽  
Cell Cycle Checkpoint ◽  
Checkpoint Pathway ◽  
Cycle Checkpoint

scholarly journals Centrosome Dynamics and Its Role in Inflammatory Response and Metastatic Process

Biomolecules ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 629
Author(s):  
Massimo Pancione ◽  
Luigi Cerulo ◽  
Andrea Remo ◽  
Guido Giordano ◽  
Álvaro Gutierrez-Uzquiza ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Rho Gtpases ◽  
Human Cancer ◽  
Genetic Disorders ◽  
Cell Cycle Checkpoint ◽  
Animal Cells ◽  
Normal Tissues ◽  
Checkpoint Pathway ◽  
New Findings ◽  
Cycle Checkpoint

Metastasis is a process by which cancer cells escape from the location of the primary tumor invading normal tissues at distant organs. Chromosomal instability (CIN) is a hallmark of human cancer, associated with metastasis and therapeutic resistance. The centrosome plays a major role in organizing the microtubule cytoskeleton in animal cells regulating cellular architecture and cell division. Loss of centrosome integrity activates the p38-p53-p21 pathway, which results in cell-cycle arrest or senescence and acts as a cell-cycle checkpoint pathway. Structural and numerical centrosome abnormalities can lead to aneuploidy and CIN. New findings derived from studies on cancer and rare genetic disorders suggest that centrosome dysfunction alters the cellular microenvironment through Rho GTPases, p38, and JNK (c-Jun N-terminal Kinase)-dependent signaling in a way that is favorable for pro-invasive secretory phenotypes and aneuploidy tolerance. We here review recent data on how centrosomes act as complex molecular platforms for Rho GTPases and p38 MAPK (Mitogen activated kinase) signaling at the crossroads of CIN, cytoskeleton remodeling, and immune evasion via both cell-autonomous and non-autonomous mechanisms.

scholarly journals An Intrinsic Cell Cycle Checkpoint Pathway Mediated by MEK and ERK in Drosophila

2006 ◽  
Vol 11 (4) ◽  
pp. 575-582 ◽  
Author(s):  
Vladic Mogila ◽  
Fan Xia ◽  
Willis X. Li
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Checkpoint ◽  
Checkpoint Pathway ◽  
Cycle Checkpoint

scholarly journals hRAD17, a structural homolog of the Schizosaccharomyces pombe RAD17 cell cycle checkpoint gene, stimulates p53 accumulation

Oncogene ◽  
1999 ◽  
Vol 18 (9) ◽  
pp. 1689-1699 ◽  
Author(s):  
Lei Li ◽  
Carolyn A Peterson ◽  
Gunilla Kanter-Smoler ◽  
Ying-Fei Wei ◽  
Louis S Ramagli ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Schizosaccharomyces Pombe ◽  
Cell Cycle Checkpoint ◽  
Checkpoint Gene ◽  
Cycle Checkpoint

Mouse Hus1, a Homolog of the Schizosaccharomyces pombe hus1+ Cell Cycle Checkpoint Gene

Genomics ◽  
1999 ◽  
Vol 59 (1) ◽  
pp. 32-39 ◽  
Author(s):  
Robert S. Weiss ◽  
Corwin F. Kostrub ◽  
Tamar Enoch ◽  
Philip Leder
Keyword(s):  
Cell Cycle ◽  
Schizosaccharomyces Pombe ◽  
Cell Cycle Checkpoint ◽  
Checkpoint Gene ◽  
Cycle Checkpoint

scholarly journals The Maize Homologue of the Cell Cycle Checkpoint Protein MAD2 Reveals Kinetochore Substructure and Contrasting Mitotic and Meiotic Localization Patterns

1999 ◽  
Vol 145 (3) ◽  
pp. 425-435 ◽  
Author(s):  
Hong-Guo Yu ◽  
Michael G. Muszynski ◽  
R. Kelly Dawe
Keyword(s):  
Cell Cycle ◽  
Spindle Assembly ◽  
Cell Cycle Checkpoint ◽  
Checkpoint Protein ◽  
Microtubule Attachment ◽  
Checkpoint Pathway ◽  
Outer Domain ◽  
Cycle Checkpoint ◽  
Mitosis And Meiosis ◽  
Meiosis I

We have identified a maize homologue of yeast MAD2, an essential component in the spindle checkpoint pathway that ensures metaphase is complete before anaphase begins. Combined immunolocalization of MAD2 and a recently cloned maize CENPC homologue indicates that MAD2 localizes to an outer domain of the prometaphase kinetochore. MAD2 staining was primarily observed on mitotic kinetochores that lacked attached microtubules; i.e., at prometaphase or when the microtubules were depolymerized with oryzalin. In contrast, the loss of MAD2 staining in meiosis was not correlated with initial microtubule attachment but was correlated with a measure of tension: the distance between homologous or sister kinetochores (in meiosis I and II, respectively). Further, the tension-sensitive 3F3/2 phosphoepitope colocalized, and was lost concomitantly, with MAD2 staining at the meiotic kinetochore. The mechanism of spindle assembly (discussed here with respect to maize mitosis and meiosis) is likely to affect the relative contributions of attachment and tension. We support the idea that MAD2 is attachment-sensitive and that tension stabilizes microtubule attachments.

RNA interference regulates the cell cycle checkpoint through the RNA export factor, Ptr1, in fission yeast

2012 ◽  
Vol 427 (1) ◽  
pp. 143-147 ◽  
Author(s):  
Tetsushi Iida ◽  
Naoko Iida ◽  
Yasuhiro Tsutsui ◽  
Fumiaki Yamao ◽  
Takehiko Kobayashi
Keyword(s):  
Cell Cycle ◽  
Rna Interference ◽  
Fission Yeast ◽  
Cell Cycle Checkpoint ◽  
Cycle Checkpoint ◽  
Rna Export

scholarly journals Interactions between p53 and MDM2 in a mammalian cell cycle checkpoint pathway.

1994 ◽  
Vol 91 (7) ◽  
pp. 2684-2688 ◽  
Author(s):  
C. Y. Chen ◽  
J. D. Oliner ◽  
Q. Zhan ◽  
A. J. Fornace ◽  
B. Vogelstein ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Mammalian Cell ◽  
Cell Cycle Checkpoint ◽  
Checkpoint Pathway ◽  
Mammalian Cell Cycle ◽  
Cycle Checkpoint

scholarly journals Separation of phenotypes in mutant alleles of the Schizosaccharomyces pombe cell-cycle checkpoint gene rad1+.

1995 ◽  
Vol 6 (12) ◽  
pp. 1793-1805 ◽  
Author(s):  
G Kanter-Smoler ◽  
K E Knudsen ◽  
G Jimenez ◽  
P Sunnerhagen ◽  
S Subramani
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Dna Replication ◽  
Schizosaccharomyces Pombe ◽  
Synthetic Lethality ◽  
Cell Cycle Checkpoint ◽  
Site Directed Mutagenesis ◽  
Restrictive Temperature ◽  
Wild Type ◽  
Cycle Checkpoint

The Schizosaccharomyces pombe rad1+ gene is involved in the G2 DNA damage cell-cycle checkpoint and in coupling mitosis to completed DNA replication. It is also required for viability when the cdc17 (DNA ligase) or wee1 proteins are inactivated. We have introduced mutations into the coding regions of rad1+ by site-directed mutagenesis. The effects of these mutations on the DNA damage and DNA replication checkpoints have been analyzed, as well as their associated phenotypes in a cdc17-K42 or a wee1-50 background. For all alleles, the resistance to radiation or hydroxyurea correlates well with the degree of functioning of checkpoint pathways activated by these treatments. One mutation, rad1-S3, completely abolishes the DNA replication checkpoint while partially retaining the DNA damage checkpoint. As single mutants, the rad1-S1, rad1-S2, rad1-S5, and rad1-S6 alleles have a wild-type phenotype with respect to radiation sensitivity and checkpoint functions; however, like the rad1 null allele, the rad1-S1 and rad1-S2 alleles exhibit synthetic lethality at the restrictive temperature with the cdc17-K42 or the wee1-50 mutation. The rad1-S5 and rad1-S6 alleles allow growth at higher temperatures in a cdc17-K42 or wee1-50 background than does wild-type rad1+, and thus behave like "superalleles." In most cases both chromosomal and multi-copy episomal mutant alleles have been investigated, and the agreement between these two states is very good. We provide evidence that the functions of rad1 can be dissociated into three groups by specific mutations. Models for the action of these rad1 alleles are discussed. In addition, a putative negative regulatory domain of rad1 is identified.

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