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Growth rate and cell size modulate the synthesis of, and requirement for, G1-phase cyclins at start
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It was shown that resveratrol can protect rodents from mammary cancer (breast cancer)18. Research shows that resveratrol exerts this protective effect by creating changes in cell creation and death in terminal ductal structures of the mammary gland18. Resveratrol exerts antioxidant and anti-inflammatory effects, and can potentially modulate cell death as well as cell cycle and estrogen receptor function in breast cancer cell lines19.
At the outset of this work, we had in mind two simple models of how Cln activity might be related to Start. The first is the critical-threshold model (Fig. ), which asserts that Start occurs when the amount of Cln rises to some critical threshold. However, because of the instability of Cln mRNA and protein, it is not clear how slowly growing cells could ever attain the same levels of Cln as rapidly growing cells, and indeed, we have shown that they do not (Fig. , , and ). We view the low level of Cln in slowly growing cells as the inevitable consequence of a combination of an unstable protein and a low rate of protein synthesis; the fact that the cells can nevertheless still pass through Start in a Cln-dependent way shows the existence of a compensatory mechanism. Thus, the critical-threshold model in its simplest form is incorrect (Fig. and ) since slowly growing and rapidly growing cells go through Start with very different amounts of Cln. Related results have previously been obtained by Heideman and coworkers (, ).
CCND2 Gene - GeneCards | CCND2 Protein | CCND2 …
While somatic cells show little developmental response to genotoxic stress, DNA damage in the germline induces both cell-cycle arrest and apoptosis (). Cell-cycle arrest is restricted to the mitotically active stem-cell population in the distal region of the gonad arms, while cell death occurs only in the meiotic pachytene regions in adult hermaphrodites. As in other eukaryotes, the RAD1 and HUS1 genes are required for checkpoint-induced arrest as well as apoptosis, together with the novel checkpoint gene / (). It is currently unclear how damage triggers cell-cycle arrest in . Neither nor Cip/Kip expression is induced in response to irradiation, which rules out one of the mechanisms used in mammals (). Other conserved mechanisms involve inactivation of Cdc25 and activation of Wee1 family members, which may mediate the arrest in .
Checkpoint controls prevent progression through cell-cycle transitions prior to the completion of critical earlier events. For instance, the cell cycle is arrested and cell death may be triggered in response to DNA damage, progress into mitosis is halted when DNA replication is ongoing, and sister-chromatid separation is delayed until all kinetochores are attached to the spindle. The DNA damage checkpoint, replication checkpoint and spindle-assembly checkpoint, respectively, impose these "brakes" on the cell cycle and couple the initiation of later events to completion of earlier events. Recent studies in have demonstrated conservation of these checkpoint pathways, identified novel components and revealed developmental functions.
IB Biology Notes – 2.5 Cell division
Developmental decisions and cell-cycle regulation interconnect at many levels and much remains to be discovered. describes proliferation in the germline, which involves some of the best characterized connections between developmental signals and cell-division control.
Despite this independence, receptiveness and response to cell-cell signaling does include a cell-cycle component. The number of VPCs adopting a vulval fate is somewhat increased in mutants, possibly because prolonged time in G1 provides greater opportunity for induction (). Different VPC fates may use a different "window of opportunity" for -mediated lateral inhibition, with the 1 versus 2 decision requiring signaling earlier than the 2 versus 3 decision (). In precocious mutants, VPCs adopt vulval fates and initiate fate-specific division patterns in L2. Dauer induction interrupts this pattern and arrests the VPC daughter cells (). Interestingly, these arrested cells lose their lineage commitment and respond as multipotent VPCs to vulval induction during post-dauer development. In all three examples, the time spent in G1 affects the VPC fate in response to signals.
Resvenox™ - Resveratrol . Polyphenolic . Antioxidant
Cellular 2 Flashcards | Quizlet
S phase - Wikipedia
Control by protein synthesis (cyclins)
Cyclin D - Wikipedia
1.6 Mitosis and Cyclins – The nature of science
Crystal structure of human cyclin D1 (blue/green) in complex with cyclin-dependent kinase 4 (yellow/red)
31/12/2017 · Excerpt
Why do the cells grown in 0.01% galactose delay budding for 2 h, until they achieve a size of 25 fl? One possibility is that Cln1 works over time and that the cells require exposure to Cln1 for a substantial period of time before its work is done; i.e., the activity of Cln is integrated over time. A second possibility is that, as cells become larger, they become more sensitive to CLN1 mRNA (e.g., by synthesizing more protein, or, alternatively, by loss of an inhibitor of Cln function). To distinguish these possibilities, we designed an experiment to obtain unbudded, Cln-less G1-phase cells of different sizes and then induce GAL-CLN1. To do this, strain BS111 was grown to mid-log phase in YEP-1% galactose-1% raffinose, washed with YEP-1% raffinose, and resuspended in YEP-1% raffinose to shut off GAL-CLN1. Subsequently, centrifugal elutriation was used to obtain small unbudded cells, exactly as for Fig. . These G1-phase cells were resuspended in YEP-1% raffinose and split into three fractions, labeled small, medium, and large. The small cells (20 fl) were further split into three aliquots, and galactose was immediately added to a final concentration of 0, 0.003, or 0.01%. The medium cells were incubated in YEP-1% raffinose at 30°C until they grew to 30 fl, and then galactose was added to a final concentration of 0, 0.003, or 0.01%. The large cells were incubated in YEP-1% raffinose at 30°C until they grew to 40 fl, and then they were treated as described above. Thus, GAL-CLN1 was turned on in the small, medium, and large cells at sizes of 20, 30, and 40 fl, respectively.
Recycling the Cell Cycle: Cyclins Revisited - ScienceDirect
Similar elutriation experiments were then done with cells grown in YEP plus 2% sucrose, 2% raffinose, or 3% ethanol, with doubling times of about 100, 130, or 220 min, respectively. In these cases, selected fractions around Start were chosen for analysis by Western blotting. Synchrony and cell cycle position were determined by the percentage of budded cells, cytometry, and α-factor resistance assays. As shown in Fig. , pre-Start cells grown in sucrose (lanes 7 to 9) had far more Cln2 than did cells grown in ethanol (lane 3) or raffinose (lanes 5 and 6) at Start (Fig. ). The pre-Start sucrose-grown cells had not yet become committed to the cell cycle (as shown by their sensitivity to α-factor arrest [Fig. , lanes 7 to 9]), and yet they had 10- to 20-fold more Cln than did ethanol-grown cells at Start (Fig. ). This shows that cells growing rapidly in sucrose require more Cln for Start than do cells growing slowly. Thus, the amount of Cln required for Start varies dramatically with the growth conditions (see Discussion).
Recycling the Cell Cycle: Cyclins ..
Goodell () first described a type of primitivestem cell, the side population (SP), in the bone marrow; thesecells were distinguished by their ability to exclude Hoechst 33342dye and they defined this characteristic as a side populationphenotype. Recently, SP cells have been considered to be CSCs inmany types of tumor tissues (). In HCC, SP cells harbor CSC-likeproperties, and they may be related to tumorigenesis, metastasisand therapeutic resistance (–). In addition, a study of the HCCcell cycle distribution showed that G cells werepresent in the SP fraction and that they may play a crucial role intumor pathogenesis (,).
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