Cyclins and the Wiring of the Yeast Cell Cycle

Futcher, Bruce

doi:10.1002/(sici)1097-0061(199612)12:16<1635::aid-yea83>3.0.co;2-o

Cited by 100 publications

(30 citation statements)

References 66 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Proliferating cells are repeating this sequence therefore the process is periodic. The eukaryotic cell division cycle is driven by an underlying molecular network which centers around complexes of cyclin-dependent kinases (Cdk's) and cyclins [2,3]. In proliferating cells the cell cycle engine is in periodic motion which suggested to many theoreticians that it is driven by a limit cycle oscillator [4-6].…”

Section: Introductionmentioning

confidence: 99%

Time scale and dimension analysis of a budding yeast cell cycle model

et al. 2006

View full text Add to dashboard Cite

Background: The progress through the eukaryotic cell division cycle is driven by an underlying molecular regulatory network. Cell cycle progression can be considered as a series of irreversible transitions from one steady state to another in the correct order. Although this view has been put forward some time ago, it has not been quantitatively proven yet. Bifurcation analysis of a model for the budding yeast cell cycle has identified only two different steady states (one for G1 and one for mitosis) using cell mass as a bifurcation parameter. By analyzing the same model, using different methods of dynamical systems theory, we provide evidence for transitions among several different steady states during the budding yeast cell cycle.

show abstract

Section: Introductionmentioning

confidence: 99%

Time scale and dimension analysis of a budding yeast cell cycle model

et al. 2006

View full text Add to dashboard Cite

show abstract

“…Homeostasis is maintained because once cells become smaller than normal, cell division again becomes dependent upon cell growth. transcription of two other G1-phase cyclins, Cln1 and Cln2 (reviewed in Nasmyth, 1993;Cross, 1995;Futcher, 1996;Mendenhall and Hodge, 1998). Cln3 activates the transcription of CLN1 and CLN2 in part by phosphorylating the yeast orthologue, Whi5, of the mammalian RB tumor suppressor gene (Costanzo et al, 2004;de Bruin et al, 2004;Schaefer and Breeden, 2004).…”

Section: Resultsmentioning

confidence: 99%

“…The ability of Cln3-Cdc28 to inactivate Whi5 is a size-dependent process (Costanzo et al, 2004;de Bruin et al, 2004;Schaefer and Breeden, 2004). But the mechanisms that link cell size to Cln3 activity are not known (reviewed in Nasmyth, 1993;Cross, 1995;Futcher, 1996;Mendenhall and Hodge, 1998). Increased transcription of CLN1 and CLN2 translates into higher Cln protein abundance, which in turn stimulates progression past Start (reviewed in Nasmyth, 1993;Cross, 1995;Futcher, 1996;Mendenhall and Hodge, 1998).…”

Section: Resultsmentioning

confidence: 99%

“…But the mechanisms that link cell size to Cln3 activity are not known (reviewed in Nasmyth, 1993;Cross, 1995;Futcher, 1996;Mendenhall and Hodge, 1998). Increased transcription of CLN1 and CLN2 translates into higher Cln protein abundance, which in turn stimulates progression past Start (reviewed in Nasmyth, 1993;Cross, 1995;Futcher, 1996;Mendenhall and Hodge, 1998). Recently, we showed that in the absence of increased transcription, Cln1 protein abundance is upregulated in a size-dependent manner .…”

Section: Resultsmentioning

confidence: 99%

“…Subsequently, it was shown that Start is analogous to the ''restriction point'' in mammalian cells (Pardee, 1974;Zetterberg et al, 1995;Blagosklonny and Pardee, 2002) (Fig 2). The archetype G1-phase CDC gene, CDC28, encodes a cyclin-dependent kinase that is required for progression past Start (reviewed in Reed et al, 1991;Reed, 1992;Nasmyth, 1993;Cross, 1995;Futcher, 1996;Mendenhall and Hodge, 1998). Importantly, CDC28 is highly conserved, and a homologue, CDC2, has been identified in all higher eukaryotes that have been examined (reviewed in Reed et al, 1991;Reed, 1992;Nasmyth, 1993;Cross, 1995;Futcher, 1996;Mendenhall and Hodge, 1998).…”

Section: Cdc Genes Cdk Cell Divisionmentioning

confidence: 99%

See 2 more Smart Citations

The Importance of Being Big

Zhang

Aguila

Schneider

et al. 2005

Journal of Investigative Dermatology Symposium Proceedings

View full text Add to dashboard Cite

The ultimate stem cell, the oocyte, is frequently very large. For example, Drosophila and Xenopus oocytes are approximately 10(5) times larger than normal somatic cells. Importantly, once the large oocytes are fertilized, the resulting embryonic cells proliferate rapidly. Moreover, these divisions occur in the absence of cell growth and are not governed by normal cell cycle controls. Observations suggest that mitogens and cell growth signals modulate proliferation by upregulating G1-phase cyclins, which in turn promote cell division. Like embryonic cells, the proliferation of cancer cells is largely independent of mitogens and growth factors. This occurs, in part, because many proteins that are known to modulate G1-phase cyclin activity are frequently mutated in cancer cells. Interestingly, we have found that both the expression and the activity of G1-phase cyclins is modulated by growth rate and cell size in yeast. These and other data suggest that proliferative capacity correlates with cell size. Thus, a major goal of our laboratory is to use yeast to investigate the relationship between proliferation rate, G1-phase cyclins, growth rate, and cell size. The elucidation of this relationship will help clarify the role of cell size in promoting proliferation in both normal and cancer cells.

show abstract

Content of endoplasmic reticulum and Golgi complex membranes positively correlates with the proliferative status of brain cells

Silvestre

Maccioni

Caputto

2008

J of Neuroscience Research

View full text Add to dashboard Cite

Although the molecular and cellular basis of particular events that lead to the biogenesis of membranes in eukaryotic cells has been described in detail, understanding of the intrinsic complexity of the pleiotropic response by which a cell adjusts the overall activity of its endomembrane system to accomplish these requirements is limited. Here we carried out an immunocytochemical and biochemical examination of the content and quality of the endoplasmic reticulum (ER) and Golgi apparatus membranes in two in vivo situations characterized by a phase of active cell proliferation followed by a phase of declination in proliferation (rat brain tissue at early and late developmental stages) or by permanent active proliferation (gliomas and their most malignant manifestation, glioblastomas multiforme). It was found that, in highly proliferative phases of brain development (early embryo brain cells), the content of ER and Golgi apparatus membranes, measured as total lipid phosphorous content, is higher than in adult brain cells. In addition, the concentration of protein markers of ER and Golgi is also higher in early embryo brain cells and in human glioblastoma multiforme cells than in adult rat brain or in nonpathological human brain cells. Results suggest that the amount of endomembranes and the concentration of constituent functional proteins diminish as cells decline in their proliferative activity.

show abstract

Cyclins and the Wiring of the Yeast Cell Cycle

Cited by 100 publications

References 66 publications

Time scale and dimension analysis of a budding yeast cell cycle model

Time scale and dimension analysis of a budding yeast cell cycle model

The Importance of Being Big

Content of endoplasmic reticulum and Golgi complex membranes positively correlates with the proliferative status of brain cells

Contact Info

Product

Resources

About