Process of Japanese macaque group fission at Arashiyama and the influences of maternal kin relations and social relations between adult males and females on it.

In 1986, the Japanese macaques of Arashiyama B group fissioned into Arashiyama E and F groups through the following process. In December 1985, the death of the beta male triggered aggressive interactions among the adult males of B group, leading to a decline in the ranks of two mid-ranked males. Several females started to gather around these two males, formed a stable subgroup (here called the female cluster), and spatially distanced themselves from other group members (main group). Some of these females had mating relations with these two males in previous mating seasons. After the end of the 1985-86 mating season, agonistic interactions occurred frequently between the female cluster and main group. Eventually, two independent groups were established. The females within the 4th degrees of matrilineal consanguinity tended to belong to the same group, but no such tendency occurred in those dyads separated by the 5th or more degrees. After the completion of group fission, mating occurred only a few times between E and F group members. In 1986, when the group fission was in progress, the birth rate of both branch groups declined, and infant mortality increased in E group. After 1987, the birth rate recovered in both branch groups although infant mortality remained high.

Elimination of the vertebrate Escherichia coli Ras-like protein homologue leads to cell cycle arrest at G1 phase and apoptosis.

Homologues of the Escherichia coli (E. coli) Ras-like protein (ERA), a GTP-binding protein with RNA binding activity, have recently been found in various species, including human, mouse, and Antirrhinum majus. Depletion of prokaryotic ERA blocks cell division without affecting chromosome segregation. However, the physiological function of eukaryotic ERA is largely unknown. We have performed a genetic analysis of chicken ERA (GdERA) in DT40 cells. Depletion of GdERA diminished the growth rate of the cells, accompanied by an accumulation of apoptotic cells. The analysis of cell cycle indicates that the elimination of GdERA caused arrest at G1 phase, but not at M phase, which highlights the distinct role of vertebrate ERA in the cell cycle progression compared to prokaryotic ERA. Furthermore, human ERA (HsERA) rescued the phenotype of GdERA-deficient cells, whereas a mutant of HsERA deprived of RNA-binding activity did not. These data suggest that vertebrate ERA regulates the G1 phase progression via an as yet unknown molecular mechanism, which involves RNA recognition by ERA.