The evolution of eusociality: no risk-return tradeoff but the ecology matters.

The origin of eusociality in the Hymenoptera is a question of major interest. Theory has tended to focus on genetic relatedness, but ecology can be just as important a determinant of whether eusociality evolves. Using the model of Fu et al. (2015), we show how ecological assumptions critically affect the conclusions drawn. Fu et al. inferred that eusociality rarely evolves because it faces a fundamental 'risk-return tradeoff'. The intuitive logic was that worker production represents an opportunity cost because it delays realising a reproductive payoff. However, making empirically justified assumptions that (1) workers take over egg-laying following queen death and (2) productivity increases gradually with each additional worker, we find that the risk-return tradeoff disappears. We then survey Hymenoptera with more specialised morphological castes, and show how the interaction between two common features of eusociality - saturating birth rates and group size-dependent helping decisions - can determine whether eusociality outperforms other strategies.

Dynamics of social queues.

Queues formed by social wasps to inherit the dominant position in the nest are analyzed by using a transient quasi-birth-and-death (QBD) process. We show that the extended nest lifespan due to division of labor between queen and helpers has a big impact on nest productivity.

Reduction of foraging work and cooperative breeding.

Using simple stochastic models, we discuss how cooperative breeders, especially wasps and bees, can improve their productivity by reducing foraging work. In a harsh environment, where foraging is the main cause of mortality, such breeders achieve greater productivity by reducing their foraging effort below full capacity, and they may thrive by adopting cooperative breeding. This could prevent the population extinction of cooperative breeders under conditions where a population of lone breeders cannot be maintained.

Sample path analysis of contribution and reward in cooperative groups.

Explaining cooperative behavior is one of the major challenges in both biology and human society. The individual reward in cooperative group depends on how we share the rewards in the group. Thus, the group size dynamics in a cooperative group and reward-allocation rule seem essential to evaluate the emergence of cooperative groups. We apply a sample path-based analysis called an extension of Little's formula to general cooperative group. We show that the expected reward is insensitive to the specific reward-allocation rule and probabilistic structure of group dynamics, and the simple productivity condition guarantees the expected reward to be larger than the average contribution. As an example, we take social queues to see the insensitivity result in detail.

Direct and indirect control of the initiation of meiotic recombination by DNA damage checkpoint mechanisms in budding yeast.

Meiotic recombination plays an essential role in the proper segregation of chromosomes at meiosis I in many sexually reproducing organisms. Meiotic recombination is initiated by the scheduled formation of genome-wide DNA double-strand breaks (DSBs). The timing of DSB formation is strictly controlled because unscheduled DSB formation is detrimental to genome integrity. Here, we investigated the role of DNA damage checkpoint mechanisms in the control of meiotic DSB formation using budding yeast. By using recombination defective mutants in which meiotic DSBs are not repaired, the effect of DNA damage checkpoint mutations on DSB formation was evaluated. The Tel1 (ATM) pathway mainly responds to unresected DSB ends, thus the sae2 mutant background in which DSB ends remain intact was employed. On the other hand, the Mec1 (ATR) pathway is primarily used when DSB ends are resected, thus the rad51 dmc1 double mutant background was employed in which highly resected DSBs accumulate. In order to separate the effect caused by unscheduled cell cycle progression, which is often associated with DNA damage checkpoint defects, we also employed the ndt80 mutation which permanently arrests the meiotic cell cycle at prophase I. In the absence of Tel1, DSB formation was reduced in larger chromosomes (IV, VII, II and XI) whereas no significant reduction was found in smaller chromosomes (III and VI). On the other hand, the absence of Rad17 (a critical component of the ATR pathway) lead to an increase in DSB formation (chromosomes VII and II were tested). We propose that, within prophase I, the Tel1 pathway facilitates DSB formation, especially in bigger chromosomes, while the Mec1 pathway negatively regulates DSB formation. We also identified prophase I exit, which is under the control of the DNA damage checkpoint machinery, to be a critical event associated with down-regulating meiotic DSB formation.

Estimating the number of double-strand breaks formed during meiosis from partial observation.

Analyzing the basic mechanism of DNA double-strand breaks (DSB) formation during meiosis is important for understanding sexual reproduction and genetic diversity. The location and amount of meiotic DSBs can be examined by using a common molecular biological technique called Southern blotting, but only a subset of the total DSBs can be observed; only DSB fragments still carrying the region recognized by a Southern blot probe are detected. With the assumption that DSB formation follows a nonhomogeneous Poisson process, we propose two estimators of the total number of DSBs on a chromosome: (1) an estimator based on the Nelson-Aalen estimator, and (2) an estimator based on a record value process. Further, we compared their asymptotic accuracy.

Reverse preferential spread in complex networks.

Large-degree nodes may have a larger influence on the network, but they can be bottlenecks for spreading information since spreading attempts tend to concentrate on these nodes and become redundant. We discuss that the reverse preferential spread (distributing information inversely proportional to the degree of the receiving node) has an advantage over other spread mechanisms. In large uncorrelated networks, we show that the mean number of nodes that receive information under the reverse preferential spread is an upper bound among any other weight-based spread mechanisms, and this upper bound is indeed a logistic growth independent of the degree distribution.

Budding yeast Pch2, a widely conserved meiotic protein, is involved in the initiation of meiotic recombination.

Budding yeast Pch2 protein is a widely conserved meiosis-specific protein whose role is implicated in the control of formation and displacement of meiotic crossover events. In contrast to previous studies where the function of Pch2 was implicated in the steps after meiotic double-strand breaks (DSBs) are formed, we present evidence that Pch2 is involved in meiotic DSB formation, the initiation step of meiotic recombination. The reduction of DSB formation caused by the pch2 mutation is most prominent in the sae2 mutant background, whereas the impact remains mild in the rad51 dmc1 double mutant background. The DSB reduction is further pronounced when pch2 is combined with a hypomorphic allele of SPO11. Interestingly, the level of DSB reduction is highly variable between chromosomes, with minimal impact on small chromosomes VI and III. We propose a model in which Pch2 ensures efficient formation of meiotic DSBs which is necessary for igniting the subsequent meiotic checkpoint responses that lead to proper differentiation of meiotic recombinants.