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The conserved fission yeast protein Rad26ATRIP preserves genomic stability by occupying central positions within DNA-structure checkpoint pathways. It is also required for proper cellular morphology, chromosome stability and following treatment with microtubule poisons. Here, we report that mutation of a putative nuclear export sequence in Rad26ATRIP disrupted its cytoplasmic localization in untreated cells and conferred abnormal cellular morphology, minichromosome instability and sensitivity to microtubule poisons without affecting DNA-structure checkpoint signaling. This mutation also disrupted a delay to spindle-pole-body separation that occurred following microtubule damage in G2. Together, these results demonstrate that Rad26ATRIP participates in two genetically defined checkpoint pathways – one that responds to genomic damage and the other to microtubule damage. This response to microtubule damage delays spindle-pole-body separation and, in doing so, might preserve both cellular morphology and chromosome stability.

Personal Rapid Transit (PRT) systems are designed so that passengers usually travel together only by choice, but strangers may choose to share a vehicle at peak times, when the system is near capacity. By predicting whether and to what extent this ride sharing will occur, PRT planners can better estimate the impact on system capacity and passenger experience. This paper develops a model for ride sharing based on queueing theory and applies it to explain the relationships between vehicle occupancy, passenger queue length and passenger waiting time. The effects of multiple destinations, passengers who are unwilling to share and passengers arriving in preformed parties are considered. A case study is provided to show how the model can be applied to a simple point-to-point system; in this case study it appears possible to reduce the size of the vehicle fleet by at least 30%, while still maintaining a high level of service for passengers during peak times.