𝔖 Bobbio Scriptorium
✦   LIBER   ✦

Benomyl resistant mutants ofSchizosaccharomyces pombecold-sensitive for mitosis

✍ Scribed by Douglas Roy; Peter A. Fantes


Book ID
104751947
Publisher
Springer-Verlag
Year
1982
Tongue
English
Weight
847 KB
Volume
6
Category
Article
ISSN
0172-8083

No coin nor oath required. For personal study only.

✦ Synopsis


S u m m a r y . We have isolated 150 benomyl resistant mutants of the fission yeast Schizosaccharomyces pombe.

Seven of these mutants were found to be cold sensitive for mitosis. These mutants were the subject of physiological, cytological and genetical characterisation. Growth and division of the seven mutants were similar to the wild type strain at 35 Β°C. After shift from the permissive (35 Β°C) to the restrictive temperature (20 Β°C) the mutants became blocked in mitosis whilst cellular growth continued. Consequently, elongate cells were formed. Six of the seven benomyl resistant mutants became blocked in mitosis at 20 Β°C with a single aberrant nucleus. In every case the benomyl resistant and cold sensitive phenotype was due to a mutation in a single nuclear gene. These mutants were found to comprise a single genetic linkage group (ben4) and were unlinked to existing TBZ/MBC resistant mutants of S. pombe. Whilst no cross resistance was found in our mutants to TBZ, six of the seven mutants were super sensitive to the spindle poison CIPC. We believe that the phenotype exhibited by these mutants is consistent with a defective tubulin subunit.

K e y w o r d s : Benomyl resistance -Y e a s t -M i t o s i s -Cell cycle mutants

I n t r o d u c t i o n

In recent years a genetical approach has been successfully used to examine the control and ordering of events in t h e eukaryotic and prokaryotic cell cycles (Nurse 1981;Simchen 1978). Mutants conditionally blocked at specif-


πŸ“œ SIMILAR VOLUMES


Mutations responsible for high light sen
✍ Diana L. Kirilovsky; Ghada Ajlani; Martine Picaud; Anne-Lise Etienne πŸ“‚ Article πŸ“… 1989 πŸ› Springer 🌐 English βš– 692 KB

The primary target of photoinhibition is the photosystem II reaction center. The process involves a reversible damage, followed by an irreversible inhibition ofphotosystem II activity. During cell exposition to high light intensity, the D 1 protein is specially degraded. An atrazine-resistant mutant