10,320 research outputs found
Telomerase-Independent Lengthening of Yeast Telomeres Occurs by an Abrupt Rap50p-Dependent, Rif-Inhibited Recombination Process
No full textEst1p as a Cell Cycle-Regulated Activator of Telomere-Bound Telomerase
No full textIn Saccharomyces cerevisiae, the telomerase components Est2p, TLC1 RNA, Est1p, and Est3p are thought to form a complex that acts late during chromosome replication (S phase) upon recruitment by Cdc13p, a telomeric DNA binding protein. Consistent with this model, we show that Est1p, Est2p, and Cdc13p are telomere-associated at this time. However, Est2p, but not Est1p, also binds telomeres before late S phase. The cdc13-2 allele has been proposed to be defective in recruitment, yet Est1p and Est2p telomere association persists in cdc13-2 cells. These findings suggest a model in which Est1p binds telomeres late in S phase and interacts with Cdc13p to convert inactive, telomere-bound Est2p to an active form
Telomere-Telomere Recombination Is an Efficient Bypass Pathway for Telomere Formation in Saccharomyces Cerevisiae
No full textShya, a Membrane Protein for Proper Septation of Hyphae in Streptomyces
No full textThe life cycle of Streptomyces involves the formation of filamentous substrate and aerial hyphae. Following cessation of growth of an aerial hypha, multiple septation occurs at the tip to produce a chain of unigenomic spores. A gene, shyA, which influences several aspects of this growth, was isolated and partially characterized in Streptomyces coelicolor. The gene product is a representative of a well- conserved family of small actinomycete proteins. The shyA mutant sporulates normally but displays hyper septum formation and altered spore-chain morphology. Biochemical separation experiments and immunofluorescence staining demonstrated that the shyA gene product locates at cell membranes. Moreover, yeast two-hybrid screen and GST-pull- down assay showed that ShyA can interact with itself. Altogether, ShyA belongs to a new family of membrane- associated proteins which plays a role in morphological differentiation in actinomycetes
Induction of Global Stress Response in Saccharomyces Cerevisiae Cells Lacking Telomerase
No full textCellular senescence is a major intermediate step from healthy cells toward tumor cells. By using microarrays that simultaneously examine the transcription levels of 6,200 Saccharomyces cerevisiae genes, we show that 45 gene transcript levels are increased and 11 are decreased after exposure to telomere shortening and cellular senescence in a telomerase- deficient mutant. About half of the genes that showed increased expression were found induced under stress, consistent with the notion that critical short telomeres cause stress to cells. Surprisingly, the expression level of telomere recombination genes was not altered suggesting that even though recombination is a means to rescue critically short telomeres, its machinery was not controlled by telomere shortening. The expression of telomere-proximal genes was also analyzed. The possibility of induction of a program to cope with cellular senescence and active telomere -telomere recombination is discussed
A New Non-Ltr Retrotransposon Provides Evidence for Multiple Distinct Site-Specific Elements in Crithidia Fasciculata Miniexon Arrays
No full textTelomere Configuration Influences the Choice of Telomere Maintenance Pathways
No full textTelomere maintenance is required for chromosome stability, and telomeres are typically replicated by the action of telomerase. In yeast cells that lack telomerase, telomeres are maintained by alternative type I and type II recombination mechanisms. Previous studies identified several proteins to control the choice between two types of recombinations. Here, we demonstrate that configuration of telomeres also plays a role to determine the fate of telomere replication in progeny. When diploid yeasts from mating equip with a specific type of telomeric structure in their genomes, they prefer to maintain this type of telomere replication in their descendants. While inherited telomere structure is easier to be utilized in progeny at the beginning stage, the telomeres in type I diploids can gradually switch to the type II cells in liquid culture. Importantly, the TLC1/tlc1 yeast cells develop type II survivors suggesting that haploid insufficiency of telomerase RNA component, which is similar to a type of dyskeratosis congenital in human. Altogether, our results suggest that both protein factors and substrate availability contribute to the choice among telomere replication pathways in yeast
Research Data for The impact of metformin on survival in diabetes patients with operable colorectal cancer: A nationwide retrospective cohort study
No full textResearch Data for The impact of metformin on survival in diabetes patients with operable colorectal cancer: A nationwide retrospective cohort study by Ping-Teng Chu, Tzu-Jung Chuang, Shu-Hung Huang, Tung-Ho Wu, Wei-Chun Huang and Jui-Ho Wang in Journal of International Medical Research</p
Rapid Cdc13 Turnover and Telomere Length Homeostasis Are Controlled by Cdk1-Mediated Phosphorylation of Cdc13
No full textBudding yeast telomerase is mainly activated by Tel1/Mec1 ( yeast ATM/ATR ) on Cdc13 from late S to G2 phase of the cell cycle. Here, we demonstrated that the telomerase-recruitment domain of Cdc13 is also phosphorylated by Cdk1 at the same cell cycle stage as the Tel1/Mec1- dependent regulation. Phosphor-specific gel analysis demonstrated that Cdk 1 phosphorylates residues 308 and 336 of Cdc13. The residue T 308 of Cdc13 is critical for efficient Mec1-mediated S306 phosphorylation in vitro. Phenotypic analysis in vivo revealed that the mutations in the Cdc13S/TP motifs phosphorylated by Cdk1 caused cell cycle delay and telomere shortening and these phenotypes could be partially restored by the replacement with a negative charge residue. In the absence of Ku or Tel1, Cdk1-mediated phosphorylation of Cdc 13 showed no effect on telomere length maintenance. Moreover , this Cdk1-mediated phosphorylation was required to promote the regular turnover of Cdc13. Together these results demonstrate that Cdk1 phosphorylates the telomerase recruitment domain of Cdc13, thereby preserves optimal function and expression level of Cdc13 for precise telomere replication and cell cycle progression
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