Protein Kinase B Gene Homologue pkbR1 Performs One of Its Roles at First Finger Stage of Dictyostelium

Author:

Ochiai Hiroshi123,Takeda Kosuke1,Fukuzawa Masashi4,Kato Atsushi156,Takiya Shigeharu356,Ohmachi Tetsuo2

Affiliation:

1. Division of Biological Sciences, Graduate School of Science, Hokkaido University, Sapporo 060-0810, Japan

2. Department of Biochemistry and Molecular Biology, Faculty of Agriculture & Life Science, Hirosaki University, 3 Bunkyo-cho, Hirosaki 036-8561, Japan

3. Division of Genome Dynamics, Creative Research Initiative Sousei, Hokkaido University, Sapporo 060-0810, Japan

4. Department of Biology, Faculty of Agriculture & Life Science, Hirosaki University, 3 Bunkyo-cho, Hirosaki 036-8561, Japan

5. Division of Functional Genome Science, Department of Biological Sciences, Graduate School of Science, Hokkaido University, Sapporo 060-0810, Japan

6. Department of Biological Sciences, Faculty of Science, Hokkaido University, Sapporo 060-0810, Japan

Abstract

ABSTRACT Dictyostelium discoideum has protein kinases AKT/PKBA and PKBR1 that belong to the AGC family of kinases. The protein kinase B-related kinase (PKBR1) has been studied with emphasis on its role in chemotaxis, but its roles in late development remained obscure. The pkbR1 null mutant stays in the first finger stage for about 16 h or longer. Only a few aggregates continue to the migrating slug stage; however, the slugs immediately go back probably to the previous first finger stage and stay there for approximately 37 h. Finally, the mutant fingers diversify into various multicellular bodies. The expression of the pkbR1 finger protein probably is required for development to the slug stage and to express ecmB , which is first observed in migrating slugs. The mutant also showed no ST-lacZ expression, which is of the earliest step in differentiation to one of the stalk cell subtypes. The pkbR1 null mutant forms a small number of aberrant fruiting bodies, but in the presence of 10% of wild-type amoebae the mutant preferentially forms viable spores, driving the wild type to form nonviable stalk cells. These results suggest that the mutant has defects in a system that changes the physiological dynamics in the prestalk cell region of a finger. We suggest that the arrest of its development is due to the loss of the second wave of expression of a protein kinase A catalytic subunit gene ( pkaC ) only in the prestalk region of the pkbR1 null mutant.

Publisher

American Society for Microbiology

Subject

Molecular Biology,General Medicine,Microbiology

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