Yeast lifespan variation correlates with cell growth and SIR2 expression.

Isogenic wild type yeast cells raised in controlled environments display a significant range of lifespan variation. Recent microfluidic studies suggest that differential growth or gene expression patterns may explain some of the heterogeneity of aging assays. Herein, we sought to complement this work by similarly examining a large set of replicative lifespan data from traditional plate assays.

Synchronization of Yeast.

The budding yeast Saccharomyces cerevisiae and fission yeast Schizosaccharomyces pombe are amongst the simplest and most powerful model systems for studying the genetics of cell cycle control. Because yeast grows very rapidly in a simple and economical media, large numbers of cells can easily be obtained for genetic, molecular, and biochemical studies of the cell cycle. The use of synchronized cultures greatly aids in the ease and interpretation of cell cycle studies.

A budding yeast's perspective on aging: the shape I'm in.

Aging is exemplified by progressive, deleterious changes that increase the probability of death. However, while the effects of age are easy to recognize, identification of the processes involved has proved to be much more difficult. Somewhat surprisingly, research using the budding yeast has had a profound impact on our current understanding of the mechanisms involved in aging.

Cell growth: when less means more.

When is less more? A new study reveals that decreased mitochondrial gene expression and reduced lipid biosynthesis may actually increase cell growth.

Identification of new cell size control genes in S. cerevisiae.

Cell size homeostasis is a conserved attribute in many eukaryotic species involving a tight regulation between the processes of growth and proliferation. In budding yeast S. cerevisiae, growth to a "critical cell size" must be achieved before a cell can progress past START and commit to cell division.

A growing role for hypertrophy in senescence.

Numerous observations support the existence of senescence factors in yeast. Historically, the asymmetric propagation and accumulation of extra-chromosomal ribosomal DNA circles (ERCs) has been proposed to fulfill this function. On the other hand, several recent papers have re-invigorated the discussion of a potential role for cell size and/or hypertrophy in yeast senescence.

FASTA barcodes: a simple method for the identification of yeast ORF deletions.

A consortium of yeast geneticists have created -6000 individual ORF deletions, representing > 96% of the currently verified or predicted ORFs in S. cerevisiae. Importantly, molecular barcodes (each a unique 20 bp sequence termed either Uptag or Downtag) were used as identifiers for every ORF deletion.

Synchronization of yeast.

The budding yeast Saccharomyces cerevisiae and fission yeast Schizosaccharomyces pombe are amongst the simplest and most powerful model systems for studying the genetics of cell cycle control. Because yeast grows very rapidly in simple and economical media, large numbers of cells can easily be obtained for genetic, molecular, and biochemical studies of the cell cycle. The use of synchronized cultures greatly aids in the ease and interpretation of cell cycle studies.

Cell size and growth rate are major determinants of replicative lifespan.

Yeast cells, like mammalian cells, enlarge steadily as they age. Unabated cell growth can promote cellular senescence; however, the significance of the relationship between size and cellular lifespan is not well understood. Herein, we report a genetic link between cell size, growth rate and lifespan.

Gene regulation: global transcription rates scale with size.

Is bigger better? Scientists have long puzzled over the potential relationship between cell size and the rate of mRNA production. A recent report builds a strong case that global transcription rates scale with size.

Glucose induction pathway regulates meiosis in Saccharomyces cerevisiae in part by controlling turnover of Ime2p meiotic kinase.

Several components of the glucose induction pathway, namely the Snf3p glucose sensor and the Rgt1p and Mth1p transcription factors, were shown to be involved in inhibition of sporulation by glucose. The glucose sensors had only a minor role in regulating transcript levels of the two key regulators of meiotic initiation, the Ime1p transcription factor and the Ime2p kinase, but a major role in regulating Ime2p stability. Interestingly, Rgt1p was involved in glucose inhibition of spore formation but not inhibition of Ime2p stability.

Ccr4 alters cell size in yeast by modulating the timing of CLN1 and CLN2 expression.

Large, multisubunit Ccr4-Not complexes are evolutionarily conserved global regulators of gene expression. Deletion of CCR4 or several components of Ccr4-Not complexes results in abnormally large cells. Since yeast must attain a critical cell size at Start to commit to division, the large size of ccr4 delta cells implies that they may have a size-specific proliferation defect.

The size of the nucleus increases as yeast cells grow.

It is not known how the volume of the cell nucleus is set, nor how the ratio of nuclear volume to cell volume (N/C) is determined. Here, we have measured the size of the nucleus in growing cells of the budding yeast Saccharomyces cerevisiae. Analysis of mutant yeast strains spanning a range of cell sizes revealed that the ratio of average nuclear volume to average cell volume was quite consistent, with nuclear volume being approximately 7% that of cell volume.

The importance of being big.

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.

Cell size and Cln-Cdc28 complexes mediate entry into meiosis by modulating cell growth.

In the yeast Saccharomyces cerevisiae, mitotic cell cycle progression depends upon the G(1)-phase cyclin-dependent kinase Cln-Cdc28 and cell growth to a minimum cell size. In contrast, Cln-Cdc28 inhibits entry into meiosis, and a cell growth requirement for sporulation has not been established. Here, we report that entry into meiosis also depends upon cell growth.

Growth rate and cell size modulate the synthesis of, and requirement for, G1-phase cyclins at start.

In Saccharomyces cerevisiae, commitment to cell cycle progression occurs at Start. Progression past Start requires cell growth and protein synthesis, a minimum cell size, and G(1)-phase cyclins. We examined the relationships among these factors.

Destructive cycles: the role of genomic instability and adaptation in carcinogenesis.

Classical theories of carcinogenesis postulate that the accumulation of several somatic mutations is responsible for oncogenesis. However, these models do not explain how non-mutagenic carcinogens cause cancer. In addition, known mutation rates appear to be insufficient to account for observed cancer rates.

Genomic scale mutant hunt identifies cell size homeostasis genes in S. cerevisiae.

Background: In most eukaryotic cells, there is a relationship between cell size and proliferative capacity. For example, in order to commit to cell division, the yeast Saccharomyces cerevisiae must attain a "critical cell size." This mechanism coordinates growth with cell division to maintain cell size homeostasis.

The CLN3/SWI6/CLN2 pathway and SNF1 act sequentially to regulate meiotic initiation in Saccharomyces cerevisiae.

Background: IME1, which is required for the initiation of meiosis, is regulated by Cln3:Cdc28 kinase, which activates the G1-to-S transition, and Snf1 kinase, which mediates glucose repression. Here we examine the pathway by which Cln3:Cdc28p represses IME1 and the relationship between Cln3:Cdc28p and Snf1p in this regulation.

Results: When wild-type yeast cease growth, they express IME1 to moderate levels, intermediate between the low levels expressed during growth and the high levels expressed during sporulation.