86 research outputs found
Event-Triggered Decentralized Federated Learning over Resource-Constrained Edge Devices
Federated learning (FL) is a technique for distributed machine learning (ML),
in which edge devices carry out local model training on their individual
datasets. In traditional FL algorithms, trained models at the edge are
periodically sent to a central server for aggregation, utilizing a star
topology as the underlying communication graph. However, assuming access to a
central coordinator is not always practical, e.g., in ad hoc wireless network
settings. In this paper, we develop a novel methodology for fully decentralized
FL, where in addition to local training, devices conduct model aggregation via
cooperative consensus formation with their one-hop neighbors over the
decentralized underlying physical network. We further eliminate the need for a
timing coordinator by introducing asynchronous, event-triggered communications
among the devices. In doing so, to account for the inherent resource
heterogeneity challenges in FL, we define personalized communication triggering
conditions at each device that weigh the change in local model parameters
against the available local resources. We theoretically demonstrate that our
methodology converges to the globally optimal learning model at a
rate under standard assumptions in distributed
learning and consensus literature. Our subsequent numerical evaluations
demonstrate that our methodology obtains substantial improvements in
convergence speed and/or communication savings compared with existing
decentralized FL baselines.Comment: 23 pages. arXiv admin note: text overlap with arXiv:2204.0372
Separase: a universal trigger for sister chromatid disjunction but not chromosome cycle progression
Separase is a protease whose liberation from its inhibitory chaperone Securin triggers sister chromatid disjunction at anaphase onset in yeast by cleaving cohesin's kleisin subunit. We have created conditional knockout alleles of the mouse Separase and Securin genes. Deletion of both copies of Separase but not Securin causes embryonic lethality. Loss of Securin reduces Separase activity because deletion of just one copy of the Separase gene is lethal to embryos lacking Securin. In embryonic fibroblasts, Separase depletion blocks sister chromatid separation but does not prevent other aspects of mitosis, cytokinesis, or chromosome replication. Thus, fibroblasts lacking Separase become highly polyploid. Hepatocytes stimulated to proliferate in vivo by hepatectomy also become unusually large and polyploid in the absence of Separase but are able to regenerate functional livers. Separase depletion in bone marrow causes aplasia and the presumed death of hematopoietic cells other than erythrocytes. Destruction of sister chromatid cohesion by Separase may be a universal feature of mitosis in eukaryotic cells
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