Unilateral Altruism in Network Routing Games with Atomic Players

We study a routing game in which one of the players unilaterally acts altruistically by taking into consideration the latency cost of other players as well as his own. By not playing selfishly, a player can not only improve the other players' equilibrium utility but also improve his own equilibrium utility. To quantify the effect, we define a metric called the Value of Unilateral Altruism (VoU) to be the ratio of the equilibrium utility of the altruistic user to the equilibrium utility he would have received in Nash equilibrium if he were selfish. We show by example that the VoU, in a game with nonlinear latency functions and atomic players, can be arbitrarily large. Since the Nash equilibrium social welfare of this example is arbitrarily far from social optimum, this example also has a Price of Anarchy (PoA) that is unbounded. The example is driven by there being a small number of players since the same example with non-atomic players yields a Nash equilibrium that is fully efficient

Incentive Mechanisms for Internet Congestion Management: Fixed-Budget Rebate versus Time-of-Day Pricing

Mobile data traffic has been steadily rising in the past years. This has generated a significant interest in the deployment of incentive mechanisms to reduce peak-time congestion. Typically, the design of these mechanisms requires information about user demand and sensitivity to prices. Such information is naturally imperfect. In this paper, we propose a \emph{fixed-budget rebate mechanism} that gives each user a reward proportional to his percentage contribution to the aggregate reduction in peak time demand. For comparison, we also study a time-of-day pricing mechanism that gives each user a fixed reward per unit reduction of his peak-time demand. To evaluate the two mechanisms, we introduce a game-theoretic model that captures the \emph{public good} nature of decongestion. For each mechanism, we demonstrate that the socially optimal level of decongestion is achievable for a specific choice of the mechanism's parameter. We then investigate how imperfect information about user demand affects the mechanisms' effectiveness. From our results, the fixed-budget rebate pricing is more robust when the users' sensitivity to congestion is "sufficiently" convex. This feature of the fixed-budget rebate mechanism is attractive for many situations of interest and is driven by its closed-loop property, i.e., the unit reward decreases as the peak-time demand decreases.Comment: To appear in IEEE/ACM Transactions on Networkin

Incentive schemes for Internet congestion management: Raffles versus time-of-day pricing

The Internet is plagued with congestion problems of growing severity which are worst at peak periods. In this paper, we compare two schemes that incentivize users to shift part of their usage from the peak-time to the off-peak time. The traditional time-of-day pricing scheme gives a fixed reward per unit of shifted usage. Conversely, the raffle-based scheme provides a random reward distributed in proportion of each user's fraction of the total shifted usage. Using a game-theoretic model, we show that both schemes can achieve an optimal level of decongestion at a unique Nash equilibrium. We provide a comparison of the schemes' sensitivity to uncertainty of the users' utilities.National Science Foundation (U.S.) (Grant CNS-0910711

Congestion pricing using a raffle-based scheme

We propose a raffle-based scheme for the decongestion of a shared resource. Our scheme builds on ideas from the economic literature on incentivizing contributions to a public good. We formulate a game-theoretic model for the decongestion problem in a setup with a finite number of users, as well as in a setup with an infinite number of non-atomic users. We analyze both setups, and show that the former converges toward the latter when the number of users becomes large. We compare our results to existing results for the public good provision problem. Overall, our results establish that raffle-based schemes are useful in addressing congestion problems.National Science Foundation (U.S.) (Grant CNS-0910711)National Science Foundation (U.S.) (Grant CCF-0424422)United States. Air Force Office of Scientific Research (FA9550-06-1-0244

Reconstitution of a 26-Subunit human kinetochore reveals cooperative microtubule binding by CENP-OPQUR and NDC80

The approximately thirty core subunits of kinetochores assemble on centromeric chromatin containing the histone H3 variant CENP-A and connect chromosomes with spindle microtubules. The chromatin proximal 16-subunit CCAN (constitutive centromere associated network) creates a mechanically stable bridge between CENP-A and the kinetochore's microtubule-binding machinery, the 10-subunit KMN assembly. Here, we reconstituted a stoichiometric 11-subunit human CCAN core that forms when the CENP-OPQUR complex binds to a joint interface on the CENP-HIKM and CENP-LN complexes. The resulting CCAN particle is globular and connects KMN and CENP-A in a 26-subunit recombinant particle. The disordered, basic N-terminal tail of CENP-Q binds microtubules and promotes accurate chromosome alignment, cooperating with KMN in microtubule binding. The N-terminal basic tail of the NDC80 complex, the microtubule-binding subunit of KMN, can functionally replace the CENP-Q tail. Our work dissects the connectivity and architecture of CCAN and reveals unexpected functional similarities between CENP-OPQUR and the NDC80 complex. [Abstract copyright: Copyright © 2018 The Author(s). Published by Elsevier Inc. All rights reserved.

Centrosome and spindle assembly checkpoint loss leads to neural apoptosis and reduced brain size

Accurate mitotic spindle assembly is critical for mitotic fidelity and organismal development. Multiple processes coordinate spindle assembly and chromosome segregation. Two key components are centrosomes and the spindle assembly checkpoint (SAC), and mutations affecting either can cause human microcephaly. In vivo studies in Drosophila melanogaster found that loss of either component alone is well tolerated in the developing brain, in contrast to epithelial tissues of the imaginal discs. In this study, we reveal that one reason for that tolerance is the compensatory relationship between centrosomes and the SAC. In the absence of both centrosomes and the SAC, brain cells, including neural stem cells, experience massive errors in mitosis, leading to increased cell death, which reduces the neural progenitor pool and severely disrupts brain development. However, our data also demonstrate that neural cells are much more tolerant of aneuploidy than epithelial cells. Our data provide novel insights into the mechanisms by which different tissues manage genome stability and parallels with human microcephaly

Architecture of the Human Ndc80-Hec1 Complex, a Critical Constituent of the Outer Kinetochore

The Ndc80 complex is a constituent of the outer plate of the kinetochore and plays a critical role in establishing the stable kinetochore-microtubule interactions required for chromosome segregation in mitosis. The Ndc80 complex is evolutionarily conserved and contains the four subunits Spc24, Spc25, Nuf2, and Ndc80 (whose human homologue is called Hec1). All four subunits are predicted to contain globular domains and extensive coiled coil regions. To gain an insight into the organization of the human Ndc80 complex, we reconstituted it using recombinant methods. The hydrodynamic properties of the recombinant Ndc80 complex are identical to those of the endogenous HeLa cell complex and are consistent with a 1:1:1:1 stoichiometry of the four subunits and a very elongated shape. Two tight Hec1-Nuf2 and Spc24-Spc25 subcomplexes, each stabilized by a parallel heterodimeric coiled coil, maintain this organization. These subcomplexes tetramerize via an interaction of the C- and N-terminal portions of the Hec1-Nuf2 and Spc24-Spc25 coiled coils, respectively. The recombinant complex displays normal kinetochore localization upon injection in HeLa cells and is therefore a faithful copy of the endogenous Ndc80 complex

Cdc20 hypomorphic mice fail to counteract de novo synthesis of cyclin B1 in mitosis

Low expression levels of Cdc20 result in chromatin bridging and chromosome misalignment, revealing a requirement for Cdc20 in efficient sister chromosome separation and chromosome–microtubule attachment