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L H Hartwell

Publications and source records attributed to L H Hartwell.

6 recordsLinked to original sources
PubMed1978

Cell division from a genetic perspective.

A novel view of the eukaryotic cell cycle is taking form as genetic strategies borrowed from investigations of microbial gene regulation and bacteriophage morphogenesis are being applied to the process of cell division. It is a genetic construct in which mutational lesions identify the primary events, thermolabile gene products reveal temporal order, mutant phenotypes yield pathways of causality, and regulatory events are localized within sequences of gene controlled steps.

Animals↗
PubMed1977

Regulation of mating in the cell cycle of Saccharomyces cerevisiae.

The capacity of haploid a yeast cells to mate (fuse with a haploid strain of alpha mating type followed by nuclear fusion to produce a diploid cell) was assessed for a variety of temperature-sensitive cell division cycle (cdc) mutants at the permissive and restrictive temperatures. Asynchronous populations of some mutants do not mate at the restrictive temperature, and these mutants define genes (cdc 1, 4, 24, and 33) that are essential both for the cell cycle and for mating. For most cdc mutants, asynchronous populations mate well at the restrictive temperature while populations synchronized at the cdc block do not. Populations of a mutant carrying the cdc 28 mutation mate well at the restrictive temperature after synchronization at the cdc 28 step. These results suggest that mating can occur from the cdc 28 step, the same step at which mating factors arrest cell cycle progress. The cell cycle interval in which mating can occur may or may not extend to the immediately succeeding and diverging steps (cdc 4 and cdc 24). High frequency mating does not occur in the interval of the cell cycle extending from the step before the initiation of DNA synthesis (cdc 7) through DNA synthesis (cdc 2, 8, and 21), medial nuclear division (cdc 13), and late nuclear division (cdc 14 and 15).

Cell Cycle↗
PubMed1977

Unequal division in Saccharomyces cerevisiae and its implications for the control of cell division.

The budding yeast, Saccharomyces cerevisiae, was grown exponentially at different rates in the presence of growth rate-limiting concentrations of a protein synthesis inhibitor, cycloheximide. The volumes of the parent cell and the bud were determined as were the intervals of the cell cycle devoted to the unbudded and budded periods. We found that S. cerevisiae cells divide unequally. The daughter cell (the cell produced at division by the bud of the previous cycle) is smaller and has a longer subsequent cell cycle than the parent cell which produced it. During the budded period most of the volume increase occurs in the bud and very little in the parent cell, while during the unbudded period both the daughter and the parent cell increase significantly in volume. The length of the budded interval of the cell cycle varies little as a function of population doubling time; the unbudded interval of the parent cell varies moderately; and the unbudded interval for the daughter cell varies greatly (in the latter case an increase of 100 min in population doubling time results in an increase of 124 min in the daughter cell's unbudded interval). All of the increase in the unbudded period occurs in that interval of G1 that precedes the point of cell cycle arrest by the S. cerevisiae alpha-mating factor. These results are qualitatively consistent with and support the model for the coordination of growth and division (Johnston, G. C., J. R. Pringle, and L. H. Hartwell. 1977. Exp. Cell. Res. 105:79-98.) This model states that growth and not the events of the DNA division cycle are rate limiting for cellular proliferation and that the attainment of a critical cell size is a necessary prerequisite for the "start" event in the DNA-division cycle, the event that requires the cdc 28 gene product, is inhibited by mating factor and results in duplication of the spindle pole body.

Cell Division↗
PubMed1976

Control of cell division in Saccharomyces cerevisiae by methionyl-tRNA.

We suggest that two events are necessary for an asynchronous population of cells to undergo arrest in the GI phase of the cell cycle upon nutrient starvation. First, passage through GI must be prevented by a deficiency of some metabolic intermediate. Since this intermediate may act indirectly to arrest division, we designate it the "signal". We have found three conditions under which Saccharomyces cerevisiae cells arrest division in GI: sulfate starvation of a prototroph, methionine starvation of an auxotroph, or a shift of a conditional methionyl-tRNA synthetase mutant [L-methionine: tRNA Met ligase (AMP-forming), EC 6.1.1.10] to a restrictive condition. We interpret these results to indicate that the signal for sulfate starvation in S. cerevisiae is generated near the end of the sulfate assimilation pathway (at or beyond the formation of mehtionyl-tRNA). As a unifying hypothesis, we propose that the signal for all nutrients is generated at the level of protein biosynthesis.

Cell Division↗